bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preferences for Oral Health States in a US Community‐Dwelling Functionally Impaired Older Adult Population: 2000–2001
Authors: Thierer Todd , Friedman Bruce 
Published: January 2009

AbstractObjectives:To determine whether and how much time in a state of ill oral health an older person would be willing to trade for optimal oral health. Methods:This is a cross‐sectional observational study of 76 subjects (52 female, 24 male) ages 47–93 (mean 75.2) recruited from a Medicare demonstration. Subjects had to need or receive help with 2+ activities of daily living (ADLs) or 3+ instrumental ADLs plus had to have had recent significant healthcare services use. A Time Trade‐Off (TTO) approach was used. TTO utility is defined as the amount of symptom‐free time (i.e., the optimal oral health state) divided by the amount of time with symptoms (either their current oral health state or the worst imaginable oral health state, depending on the scenario), at the point of indifference (the point past which the person is unwilling to trade additional life expectancy). Results:When starting from their current oral health state, 39% of the subjects were willing to exchange time resulting in a shorter life with optimal oral health. Theywere willing to trade 14.0 months of life on average and valued each year in their current oral health state as 91% of a year in optimal oral health. When starting in the poorest oral health state, 79% of the subjects were willing to accept a shorter life. They were willing to trade 33.7 months of life on average, and valued the poorest state as worth 79% of a year in optimal oral health. Conclusions:Dentists should take into consideration this group's preference for optimal oral health.
Infection Control Measures Among Senior Dental Students in Rio de Janeiro State, Brazil
Authors: de Souza Rogério A. , Namen Fátima M. , Jr Joāo Galan , Vieira Cristine , Sedano Heddie O. 
Published: January 2009

AbstractObjectives:The aim of this study was to verify the practices and attitudes of senior dental students about infection control procedures. Methods:A cross‐sectional survey was performed during the 1st semester of 2003. Open‐ and close‐ended questions were given to 196 students in 6 universities. Results:Overall, 90.8% of students had been vaccinated for hepatitis B. Only 25.0% have been assessed for anti‐HBs. A total of 99.5% students reported always using gloves for all procedures. Eye protection were always used by 84.2% of students, and all the students used face masks for all procedures. Caps or hair covers were used by 92.3% of students and 87.8% reported no objection to treating patients with infectious diseases. Among instructors, the students observed that 60.2% of them did not use gloves for all procedures, 43.4% of those didn't change gloves between patients. Conclusions:These results address the need for an improved quality assurance, in order for the students and faculty to improve their practices and attitudes on infection control measures.
Faciogenital Dysplasia Protein Fgd1 Regulates Invadopodia Biogenesis and Extracellular Matrix Degradation and Is Up-regulated in Prostate and Breast Cancer
Authors: Ayala Inmaculada , Giacchetti Giada , Caldieri Giusi , Attanasio Francesca , Mariggiò Stefania , Tetè Stefano , Polishchuk Roman , Castronovo Vincent , Buccione Roberto 
Published: January 2009

Abstract
Invadopodia are proteolytically active membrane protrusions that extend from the ventral surface of invasive tumoral cells grown on an extracellular matrix (ECM). The core machinery controlling invadopodia biogenesis is regulated by the Rho GTPase Cdc42. To understand the upstream events regulating invadopodia biogenesis, we investigated the role of Fgd1, a Cdc42-specific guanine nucleotide exchange factor. Loss of Fgd1 causes the rare inherited human developmental disease faciogenital dysplasia. Here, we show that Fgd1 is required for invadopodia biogenesis and ECM degradation in an invasive cell model and functions by modulation of Cdc42 activation. We also find that Fgd1 is expressed in human prostate and breast cancer as opposed to normal tissue and that expression levels matched tumor aggressiveness. Our findings suggest a central role for Fgd1 in the focal degradation of the ECM in vitro and, for the first time, show a connection between Fgd1 and cancer progression, proposing that it might function during tumorigenesis. [Cancer Res 2009;69(3):747–52]
Transcriptional Repression of Epithelial Cell Adhesion Molecule Contributes to p53 Control of Breast Cancer Invasion
Authors: Sankpal Narendra V. , Willman Michael W. , Fleming Timothy P. , Mayfield John D. , Gillanders William E. 
Published: January 2009

Abstract
p53 is a tumor suppressor gene with well-characterized roles in cell cycle regulation, apoptosis, and maintenance of genome stability. Recent evidence suggests that p53 may also contribute to the regulation of migration and invasion. Epithelial cell adhesion molecule (EpCAM) is a transmembrane glycoprotein that is overexpressed in the majority of human epithelial carcinomas, including breast and colorectal carcinomas. We show by chromatin immunoprecipitation assays that p53 interacts with a candidate p53 binding site within the EpCAM gene. p53-mediated transcriptional repression of EpCAM was confirmed in gain-of-function and loss-of-function experimental systems. Induction of wild-type p53 was associated with a significant dose-dependent decrease in EpCAM expression; conversely, specific ablation of p53 was associated with a significant increase in EpCAM expression. At the functional level, specific ablation of p53 expression is associated with increased breast cancer invasion, and this effect is abrogated by concomitant specific ablation of EpCAM expression. Taken together, these biochemical and functional data are the first demonstration that (a) wild-type p53 protein binds to a response element within the EpCAM gene and negatively regulates EpCAM expression, and (b) transcriptional repression of EpCAM contributes to p53 control of breast cancer invasion. [Cancer Res 2009;69(3):753–7]
Intakes of Red Meat, Processed Meat, and Meat Mutagens Increase Lung Cancer Risk
Authors: Lam Tram Kim , Cross Amanda J. , Consonni Dario , Randi Giorgia , Bagnardi Vincenzo , Bertazzi Pier Alberto , Caporaso Neil E. , Sinha Rashmi , Subar Amy F. , Landi Maria Teresa 
Published: January 2009

Abstract
Red and processed meat intake may increase lung cancer risk. However, the epidemiologic evidence is inconsistent and few studies have evaluated the role of meat mutagens formed during high cooking temperatures. We investigated the association of red meat, processed meat, and meat mutagen intake with lung cancer risk in Environment And Genetics in Lung cancer Etiology, a population-based case-control study. Primary lung cancer cases (n = 2,101) were recruited from 13 hospitals within the Lombardy region of Italy examining ∼80% of the cases from the area. Noncancer population controls (n = 2,120), matched to cases on gender, residence, and age, were randomly selected from the same catchment area. Diet was assessed in 1,903 cases and 2,073 controls and used in conjunction with a meat mutagen database to estimate intake of heterocyclic amines (HCA) and benzo(a)pyrene (BaP). Multivariable odds ratios (OR) and 95% confidence intervals (95% CI) for sex-specific tertiles of intake were calculated using unconditional logistic regression. Red and processed meat were positively associated with lung cancer risk (highest-versus-lowest tertile: OR, 1.8; 95% CI, 1.5–2.2; P trend &lt; 0.001 and OR, 1.7; 95% CI, 1.4–2.1; P trend &lt; 0.001, respectively); the risks were strongest among never smokers (OR, 2.4; 95% CI, 1.4–4.0; P trend = 0.001 and OR, 2.5; 95% CI, 1.5–4.2; P trend = 0.001, respectively). HCAs and BaP were significantly associated with increased risk of lung cancer. When separated by histology, significant positive associations for both meat groups were restricted to adenocarcinoma and squamous cell carcinoma but not small cell carcinoma of the lung. In summary, red meat, processed meat, and meat mutagens were independently associated with increased risk of lung cancer. [Cancer Res 2009;69(3):932–9]
Collagens in the progression and complications of atherosclerosis
Authors: Adiguzel Eser , Ahmad Pamela J , Franco Christopher , Bendeck Michelle P 
Published: January 2009

Abstract Collagens constitute a major portion of the extracellular matrix in the atherosclerotic plaque, where they contribute to the strength and integrity of the fibrous cap, and also modulate cellular responses via specific receptors and signaling pathways. This review focuses on the diverse roles that collagens play in atherosclerosis; regulating the infiltration and differentiation of smooth muscle cells and macrophages; controlling matrix remodeling through feedback signaling to proteinases; and influencing the development of atherosclerotic complications such as plaque rupture, aneurysm formation and calcification. Expanding our understanding of the pathways involved in cell–matrix interactions will provide new therapeutic targets and strategies for the diagnosis and treatment of atherosclerosis.
The role of optical coherence tomography in vascular medicine
Authors: Farooq Muhammad U , Khasnis Atul , Majid Arshad , Kassab Mounzer Y 
Published: January 2009

Abstract Optical coherence tomography (OCT) is an emerging imaging modality that provides high-resolution, microstructural information on atherosclerotic plaques in biological systems. Intracoronary OCT can identify thin-cap fibroatheroma and other vulnerable plaques that may be responsible for acute coronary events. These characteristics make OCT helpful in guiding coronary management and interventions, including stent apposition and early identification of procedure-related complications. OCT is being assessed for its potential role in carotid plaque characterization and in the diagnosis of peripheral arterial atherosclerosis. Its current use in studying carotid and cerebral vasculature and in the diagnosis of peripheral arterial diseases is limited and ill defined, but it is finding increasing application in these areas. Its performance can be further improved by increasing the signal to noise ratio and by using dynamic focus tracking techniques. It can potentially be used to monitor the progression and regression of atherosclerosis in the coronary, cerebral and peripheral vasculature. New indications for its use in vascular medicine are emerging as its technology continues to improve over time.
Endovascular treatment of septic thrombophlebitis: a case report of a rare complication and review of the literature
Authors: Schifferdecker Branislav , Merchán Juan Andrés , Ahmar Corinne , Worthington Michael , Griben Andre , Schainfeld Robert M , Soukas Peter A 
Published: January 2009

Abstract We report a case of severe deep venous thrombosis (DVT) treated with multimodality therapy that was complicated by sepsis due to thrombus likely infected by Salmonella virchow. We review the current therapeutic options in the therapy of severe DVT and cardiovascular pathology associated with non-typhoid Salmonella.
Estradiol-induced, endothelial progenitor cell-mediated neovascularization in male mice with hind-limb ischemia
Authors: Ruifrok Willem-Peter T , de Boer Rudolf A , Iwakura Atsushi , Silver Marcy , Kusano Kengo , Tio Rene A , Losordo Douglas W 
Published: January 2009

Abstract We investigated whether administration of estradiol to male mice augments mobilization of bone marrow-derived endothelial progenitor cells (EPC) and incorporation into foci of neovascularization after hind-limb ischemia, thereby contributing to blood flow restoration. Mice were randomized and implanted with placebo pellets or pellets containing low-dose estradiol (0.39 mg) or high-dose estradiol (1.7 mg). Hind-limb ischemia was induced by unilateral resection of the left femoral artery 1 week after pellet implantation, then EPC mobilization and functional recovery was evaluated. EPC recruitment was assessed in mice transplanted with bone marrow from transgenic donors expressing β-galactosidase driven by the Tie-2 promoter. EPC culture assay performed 2 weeks after pellet implantation revealed a significantly greater ( p < 0.05) number of circulating EPCs in the high-dose estradiol group than in the low-dose estradiol and placebo groups. At 3 and 4 weeks after induction of hind-limb ischemia, perfusion was significantly greater ( p < 0.05) in high-dose estradiol mice than in mice implanted with the low-dose estradiol or placebo pellets. At 1 and 4 weeks after hind-limb ischemia surgery, more bone marrow-derived EPCs, identified as β-galactosidase-positive cells, were observed in ischemic regions from high-dose estradiol animals than in low-dose ( p < 0.05) or placebo groups ( p < 0.05). These results indicate that estradiol dose-dependently increases the levels of EPCs in peripheral blood in male animals, improves the recovery of blood flow, and decreases limb necrosis after hind-limb ischemia, and that this enhancement occurs, in part, through augmentation of EPC mobilization and greater incorporation of bone marrow-derived EPCs into foci of neovascularization.
Dual roles of tumor necrosis factor-α receptor-1 in a mouse model of hindlimb ischemia
Authors: Jiang Jun , Wang Jianan , Li Changling , Yu Shan Ping , Wei Ling 
Published: January 2009

Abstract Signals in the tumor necrosis factor α (TNF-α) pathway are upregulated after ischemia, yet its role in peripheral ischemia remains unclear. We investigated the effect of TNF-α receptor 1 (TNFR-1) in acute limb ischemia of TNFR-1 knockout (TNFR-1–/–) and wild type (WT, TNFR-1+/+) mice. Laser Doppler scanning showed that although pre-ischemia blood flow levels were similar in these mice, the limb reperfusion after ischemia was significantly higher in TNFR-1–/– mice 1–7 days after injury. Consistently, fewer TUNEL-positive cells, less DNA fragmentation, and a lower ischemic score were detected in the TNFR-1–/– group when compared to WT controls. Western blot analysis revealed less expression of pro-apoptotic markers Bax and cleaved caspase-3 in TNFR-1–/– mice 1 day after ischemia, supporting the hypothesis that the absence of TNFR-1 results in a reduction of apoptosis. The rate of post-ischemia amputation was 50% in WT mice versus 0% in TNFR-1–/– mice. However, immunohistochemical co-staining of microvessel marker CD31 and cellular proliferation marker BrdU 21 days after ischemia showed an impaired angiogenic activity in the TNFR-1–/– mice. These data were supported by Western blot analysis, which indicated a decreased expression of angiopoietin-1 (Ang-1) and its receptor Tie-2 in TNFR-1–/– mice. Our results suggest that a deficiency in TNFR-1 prevents the activation of death-related proteins downstream to TNF-α and attenuates apoptosis in acute limb ischemia, but the lack of TNFR-1 signaling hinders the belated angiogenesis mediated by the Ang-1/Tie-2 pathway.
Regions of acquired uniparental disomy at diagnosis of follicular lymphoma are associated with both overall survival and risk of transformation
Authors: O'Shea Derville , O'Riain Ciarán , Gupta Manu , Waters Rachel , Yang Youwen , Wrench David , Gribben John , Rosenwald Andreas , Ott German , Rimsza Lisa M. , Holte Harald , Cazier Jean-Baptiste , Johnson Nathalie A. , Campo Elias , Chan Wing C. , Gascoyne Randy D. , Young Bryan D. , Staudt Louis M. , Lister T. Andrew , Fitzgibbon Jude 
Published: January 2009

AbstractAcquired homozygosity in the form of segmental acquired uniparental disomy (aUPD) has been described in follicular lymphoma (FL) and is usually due to mitotic recombination. SNP array analysis was performed with the use of the Affymetrix 10K 2.0 Gene-chip array on DNA from 185 diagnostic FL patients to assess the prognostic relevance of aUPD. Genetic abnormalities were detected in 118 (65%) of 182 patients. Number of abnormalities was predictive of outcome; more than 3 abnormalities was associated with inferior overall survival (OS; P < .03). Sites of recurrent aUPD were detected on 6p (n = 25), 16p (n = 22), 12q (n = 17), 1p36 (n = 14), 10q (n = 8), and 6q (n = 8). On multivariate analysis aUPD on 1p36 correlated with shorter OS (P = .05). aUPD on 16p was predictive of transformation (P = .03) and correlated with poorer progression-free survival (P = .02). aUPD is frequent at diagnosis of FL and affects probability of disease transformation and clinical outcome.
BioMart – biological queries made easy
Authors: Smedley Damian , Haider Syed , Ballester Benoit , Holland Richard , London Darin , Thorisson Gudmundur , Kasprzyk Arek 
Published: January 2009

Abstract

Background
Biologists need to perform complex queries, often across a variety of databases. Typically, each data resource provides an advanced query interface, each of which must be learnt by the biologist before they can begin to query them. Frequently, more than one data source is required and for high-throughput analysis, cutting and pasting results between websites is certainly very time consuming. Therefore, many groups rely on local bioinformatics support to process queries by accessing the resource's programmatic interfaces if they exist. This is not an efficient solution in terms of cost and time. Instead, it would be better if the biologist only had to learn one generic interface. BioMart provides such a solution.

Results
BioMart enables scientists to perform advanced querying of biological data sources through a single web interface. The power of the system comes from integrated querying of data sources regardless of their geographical locations. Once these queries have been defined, they may be automated with its "scripting at the click of a button" functionality. BioMart's capabilities are extended by integration with several widely used software packages such as BioConductor, DAS, Galaxy, Cytoscape, Taverna. In this paper, we describe all aspects of BioMart from a user's perspective and demonstrate how it can be used to solve real biological use cases such as SNP selection for candidate gene screening or annotation of microarray results.

Conclusion
BioMart is an easy to use, generic and scalable system and therefore, has become an integral part of large data resources including Ensembl, UniProt, HapMap, Wormbase, Gramene, Dictybase, PRIDE, MSD and Reactome. BioMart is freely accessible to use at http://www.biomart.org.
Combining chemical genomics screens in yeast to reveal spectrum of effects of chemical inhibition of sphingolipid biosynthesis
Authors: Kemmer Danielle , McHardy Lianne M , Hoon Shawn , Rebérioux Delphine , Giaever Guri , Nislow Corey , Roskelley Calvin D , Roberge Michel 
Published: January 2009

Abstract

Background
Single genome-wide screens for the effect of altered gene dosage on drug sensitivity in the model organism Saccharomyces cerevisiae provide only a partial picture of the mechanism of action of a drug.

Results
Using the example of the tumor cell invasion inhibitor dihydromotuporamine C, we show that a more complete picture of drug action can be obtained by combining different chemical genomics approaches – analysis of the sensitivity of ρ
0 cells lacking mitochondrial DNA, drug-induced haploinsufficiency, suppression of drug sensitivity by gene overexpression and chemical-genetic synthetic lethality screening using strains deleted of nonessential genes. Killing of yeast by this chemical requires a functional mitochondrial electron-transport chain and cytochrome c heme lyase function. However, we find that it does not require genes associated with programmed cell death in yeast. The chemical also inhibits endocytosis and intracellular vesicle trafficking and interferes with vacuolar acidification in yeast and in human cancer cells. These effects can all be ascribed to inhibition of sphingolipid biosynthesis by dihydromotuporamine C.

Conclusion
Despite their similar conceptual basis, namely altering drug sensitivity by modifying gene dosage, each of the screening approaches provided a distinct set of information that, when integrated, revealed a more complete picture of the mechanism of action of a drug on cells.
Identification of ATP synthase beta subunit (ATPB) on the cell surface as a non-small cell lung cancer (NSCLC) associated antigen
Authors: Lu Ze-jun , Song Qi-fang , Jiang Sa-sa , Song Qi , Wang Wei , Zhang Gao-hua , Kan Bin , Gou Lan-tu , Chen Li-juan , Luo Feng , Qian Zhi Yong , Yang Jin-liang , Wei Yu Quan 
Published: January 2009

Abstract

Background
Antibody-based immuneotherapy has achieved some success for cancer. But the main problem is that only a few tumor-associated antigens or therapeutic targets have been known to us so far. It is essential to identify more immunogenic antigens (especially cellular membrane markers) for tumor diagnosis and therapy.

Methods
The membrane proteins of lung adenocarcinoma cell line A549 were used to immunize the BALB/c mice. A monoclonal antibody 4E7 (McAb4E7) was produced with hybridoma technique. MTT cell proliferation assay was carried out to evaluate the inhibitory effect of McAb4E7 on A549 cells. Flow cytometric assay, immunohistochemistry, western blot and proteomic technologies based on 2-DE and mass spectrometry were employed to detect and identify the corresponding antigen of McAb4E7.

Results
The monoclonal antibody 4E7 (McAb4E7) specific against A549 cells was produced, which exhibited inhibitory effect on the proliferation of A549 cells. By the proteomic technologies, we identified that ATP synthase beta subunit (ATPB) was the corresponding antigen of McAb4E7. Then, flow cytometric analysis demonstrated the localization of the targeting antigen of McAb4E7 was on the A549 cells surface. Furthermore, immunohistochemstry showed that the antigen of McAb4E7 mainly aberrantly expressed in tumor cellular membrane in non-small cell lung cancer (NSCLC), but not in small cell lung cancer (SCLC). The rate of ectopic expressed ATPB in the cellular membrane in lung adenocarcinoma, squamous carcinoma and their adjacent nontumourous lung tissues was 71.88%, 66.67% and 25.81% respectively.

Conclusion
In the present study, we identified that the ectopic ATPB in tumor cellular membrane was the non-small cell lung cancer (NSCLC) associated antigen. ATPB may be a potential biomarker and therapeutic target for the immunotherapy of NSCLC.
Freund's vaccine adjuvant promotes Her2/Neu breast cancer
Authors: Cotroneo Michelle S , Haag Jill D , Stapel Nicholas R , Waller Jordy L , Woditschka Stephan , Gould Michael N 
Published: January 2009

Abstract

Background
Inflammation has been linked to the etiology of many organ-specific cancers. Indirect evidence suggests a possible role for inflammation in breast cancer. We investigated whether the systemic inflammation induced by Freund's adjuvant (FA) promotes mammary carcinogenesis in a rat model in which cancer is induced by the neu oncogene.

Methods
The effects of FA on hyperplastic mammary lesions and mammary carcinomas were determined in a neu-induced rat model. The inflammatory response to FA treatment was gauged by measuring acute phase serum haptoglobin. In addition, changes in cell proliferation and apoptosis following FA treatment were assessed.

Results
Rats receiving FA developed twice the number of mammary carcinomas as controls. Systemic inflammation following FA treatment is chronic, as shown by a doubling of the levels of the serum biomarker, haptoglobin, 15 days following initial treatment. We also show that this systemic inflammation is associated with the increased growth of hyperplastic mammary lesions. This increased growth results from a higher rate of cellular proliferation in the absence of changes in apoptosis.

Conclusion
Our data suggests that systemic inflammation induced by Freund's adjuvant (FA) promotes mammary carcinogenesis. It will be important to determine whether adjuvants currently used in human vaccines also promote breast cancer.