bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fluoride content of commercially‐available bottled water in Bangkok, Thailand
Authors: Dhanuthai Kittipong , Thangpisityotin Malee 
Published: February 2011

AbstractAim:  To determine the fluoride content of commercially‐available bottled water in Bangkok.Methods:  Thirty brands of bottled water (17 bottled plain water and 13 bottled mineral water) were obtained from supermarkets in Bangkok. Two randomly‐selected samples of each brand were purchased 6 months apart. A 5‐mL sample was mixed with 5 mL of total ionic‐strength adjusting buffer III. The fluoride content of each sample was determined in triplicate by a fluoride ion‐selective electrode. Fluoride standards ranging in concentration from 0.01 to 1.00 ppm were used to calibrate the measurements. Data were analyzed by Statistical Package for the Social Sciences software, version 13.0.Results:  The fluoride content of bottled water in Bangkok ranged from 0.03 to 0.72 ppm, with a mean ± standard deviation of 0.17 ± 0.16 ppm. The mean fluoride content of bottled mineral water was slightly higher than that of bottled plain water, but the difference was not statistically significant.Conclusions:  Most commercially‐available bottled water in Bangkok contains negligible amounts of fluoride. This serves as baseline data for dentists prescribing a fluoride supplement to make the utmost use of the fluoride caries preventive effect, while avoiding adverse effects, such as dental fluorosis.
Tobacco sales and promotion in bars, cafes and nightclubs from large cities around the world
Authors: Shahrir Shahida , Wipfli Heather , Avila-Tang Erika , Breysse Patrick N , Samet Jonathan M , Navas-Acien Ana ,   the FAMRI Bar Study Investigators
Published: February 2011

ContextLittle is known about tobacco promotion activities in low and middle-income countries. Information on tobacco sales, advertisement and promotion in bars, cafes and nightclubs is needed to develop interventions to reduce smoking initiation and relapse, particularly among youths and young adults.ObjectiveTo evaluate cigarette sales and tobacco advertisement and promotion in bars, cafes and nightclubs using a volunteer survey approach in large cities throughout the world.MethodsBetween 2007 and 2009, we administered an interview-based survey to 231 bar/cafe/nightclub owners/managers in 24 large cities in Africa, the Americas, Asia and eastern Europe.ResultsCigarette sales and tobacco advertisement and promotions were found in bars/cafes/nightclubs in most cities. Examples of promotions included cigarette giveaways and event sponsorship. Establishments that allowed smoking were more likely to sell cigarettes compared to smoke-free establishments (OR 8.67, 95% CI 3.25 to 23.1). Larger establishments (maximum occupancy ≥100 vs <100 customers) were more likely to have tobacco advertising (OR 4.35, 95% CI 2.04 to 9.24) and to receive promotional items from tobacco companies (OR 3.18, 95% CI 1.41 to 7.17).ConclusionsCigarette sales and tobacco promotions were common in bars, cafes and nightclubs in the majority of cities. Socialising and hospitality venues must be covered by legislation banning tobacco sales and promotions to limit exposure among populations at high risk of tobacco initiation and relapse from quitting.
DILEPTON PRODUCTION STUDIED WITH THE HADES SPECTROMETER
Authors:   HADES Collaboration, RUSTAMOV A. , AGAKISHIEV G. , BALANDA A. , BELVER D. , BELYAEV A. , BLANCO A. , BÖHMER M. , BOYARD J. L. , CABANELAS P. , CASTRO E. , CHERNENKO S. , DÍAZ J. , DYBCZAK A. , EPPLE E. , FABBIETTI L. , FATEEV O. , FINOCCHIARO P. , FONTE P. , FRIESE J. , FRÖHLICH I. , GALATYUK T. , GARZÓN J. A. , GIL A. , GOLUBEVA M. , GONZÁLEZ-DÍAZ D. , GUBER F. , GUMBERIDZE M. , HENNINO T. , HOLZMANN R. , HUCK P. , IERUSALIMOV A. , IORI I. , IVASHKIN A. , JURKOVIC M. , KÄMPFER B. , KARAVICHEVA T. , KOENIG I. , KOENIG W. , KOLB B. W. , KOPP A. , KORCYL G. , KORNAKOV G. K. , KOTTE R. , KOZUCH A. , KRÁSA A. , KRIZEK F. , KRÜCKEN R. , KUC H. , KÜHN W. , KUGLER A. , KUREPIN A. , KURILKIN A. , KURILKIN P. , KÄHLITZ P. , LADYGIN V. , LAMAS-VALVERDE J. , LANG S. , LAPIDUS K. , LIU T. , LOPES L. , LORENZ M. , MAIER L. , MANGIAROTTI A. , MARKERT J. , METAG V. , MICHALSKA B. , MICHEL J. , MÜNTZ C. , NAUMANN L. , PACHMAYER Y. C. , PALKA M. , PARPOTTAS Y. , PECHENOV V. , PECHENOVA O. , PIETRASZKO J. , PRZYGODA W. , RAMSTEIN B. , RESHETIN A. , ROSKOSS J. , SADOVSKY A. , SALABURA P. , SCHMAH A. , SIEBENSON J. , SOBOLEV YU. G. , SPATARO S. , STRÖBELE H. , STROTH J. , STURM C. , TARANTOLA A. , TEILAB K. , TLUSTY P. , TRAXLER M. , TREBACZ R. , TSERTOS H. , VASILIEV T. , WAGNER V. , WEBER M. , WÜSTENFELD J. , YUREVICH S. , ZANEVSKY Y. 
Published: February 2011

With the HADES spectrometer at GSI we have studied dilepton production in various collision systems from elementary N + N , over p + A , up to the medium-heavy Ar + KCl system. We have confirmed the puzzling results of the former DLS collaboration at the Bevalac. While we have traced the origin of the excess pair yield in C + C collisions to elementary p + p and n + p processes, we find a significant contribution from the dense phase of the collision in larger Ar + KCl system. From recently obtained e + e - pair spectra in p + p and p + Nb interactions at 3.5 GeV kinetic beam energy the inclusive production cross sections for neutral pions, η , ω and ρ mesons are extracted for the first time at this beam energy. Furthermore, the production mechanisms of the vector mesons, which are not known at these energies, are investigated. The direct comparison of p + p and p + Nb data allows us to investigate in-medium mass modifications of vector mesons at nuclear ground state density. On the other hand, exclusive production of ω and η mesons in p + p reactions at 3.5 GeV were studied via their π+π-π0 decay channel. Production cross sections and angular distributions for both states were determined.
ELENA: AN UPGRADE TO THE ANTI-PROTON DECELERATOR AT CERN
Authors: OELERT WALTER 
Published: February 2011

CERN has a long tradition of pursuing fundamental physics on a variety of energy scales. For anti-protons CERN famously produced the high-energy SPS beam but also the world's only and unique sources of low-energy anti-protons – first the Low Energy Anti-proton Ring (LEAR) and thereafter the Anti-proton Decelerator (AD). The scientific demand for low-energy anti-protons at the AD continues to grow. More rapid progress and much higher measurement precision might be possible by upgrading the AD to increase and optimize the number of cold anti-protons that can be trapped and accumulated. To achieve this the construction of an Extra Low ENergy Antiproton (ELENA) ring is proposed which involves both the addition of a small storage ring and electrostatic beam lines to the experiments. The design parameters have been carefully studied and agreed upon over several years. At least during the next decade there is no alternative low-energy anti-proton source for physics to be done now.
WAYS TO MAKE POLARIZED ANTIPROTON BEAMS
Authors: KILIAN K. , GRZONKA D. , MÖHL D. , OELERT W. 
Published: February 2011

For making polarized antiproton beams the so called filter method is normally discussed. It is based on the depletion of one spin component due to the spin dependent interaction if a stored beam passes a polarized target. The method has been proven by the FILTEX collaboration and detailed studies are presently performed by the PAX collaboration. Another source for polarized antiprotons is the antilambda decay as it was used in the only experiment with polarized antiprotons so far at FERMILAB. Furthermore the antiproton production process itself if showing polarisation, would be by far the best way to get polarized [Formula: see text]. It can be assumed to result from a quasi-free proton-nucleon collison. Up to now it has never been investigated in detail. In such a hadronic interaction the antiprotons may have substantial polarisation which would simplify the preparation of a polarized antiproton beam drastically. It is proposed to measure the polarisation of antiprotons produced in a fixed target experiment.
Targeting Ovarian Tumor Cell Adhesion Mediated by Tissue Transglutaminase
Authors: Khanna May , Chelladurai Bhadrani , Gavini Aruna , Li Liwei , Shao Minghai , Courtney David , Turchi John J. , Matei Daniela , Meroueh Samy 
Published: February 2011

Abstract
Tissue transglutaminase (TG2) is a transpeptidase involved in protein cross-linking through generation of ϵ-(γ-glutamyl)lysine isopeptide bonds. It also promotes cell adhesion through interaction with fibronectin and facilitates formation of fibronectin–integrin complexes. This interaction is involved in tumor cell adhesion to the matrix and in the process of tumor dissemination. Its inhibition by small molecules may therefore be useful in blocking metastasis. To that end, we screened more than 800,000 compounds following an in silico docking approach targeting two distinct cavities in the vicinity of the fibronectin-binding site on TG2. A total of 120 compounds were acquired and tested in cell culture–based assays for inhibition of ovarian tumor cell adhesion and proliferation. Seven compounds showed more than 50% inhibition of cell adhesion at a concentration of 25 μmol/L. A follow-up fluorescence polarization study revealed that one compound in particular (ITP-79) inhibited binding of a TG2 peptide to a 42-kDa fragment of fibronectin in a dose-dependent manner. This inhibition was confirmed in cancer cells by coimmunoprecipitation. A competition assay with surface plasmon resonance showed that ITP-79 modulated binding of TG2 to fibronectin. Direct binding of compounds that inhibited adhesion to TG2 were examined with differential scanning fluorimetry, which measures the effect of the compound on the melting temperature of the target. Two compounds, including ITP-79, reduced TG2 stabilization, mimicking the effects of GTP, a known negative allosteric regulator of TG2 enzymatic function. This suggests a potential allosteric mechanism for the compound in light of its distal target site. Mol Cancer Ther; 10(4); 626–36. ©2011 AACR.
Advances in imaging angiogenesis and inflammation in atherosclerosis
Authors: Zagorchev Lyubomir , Mulligan-Kehoe Mary Jo 
Published: February 2011

SummaryAdvances in imaging technology have provided powerful tools for dissecting the angiogenic and inflammatory aspects of atherosclerosis. Improved technology along with multi-modal approaches has expanded the utilisation of imaging. Recent advances provide the ability to better define structure and development of angiogenic vessels, identify relationships between inflammatory mediators and the vessel wall, validate biological effects of anti-inflammatory and anti-angiogenic drugs, delivery and/or targeting specific molecules to inflammatory regions of atherosclerotic plaques.
Nod1 Ligands Induce Site-Specific Vascular Inflammation
Authors: Nishio Hisanori , Kanno Shunsuke , Onoyama Sagano , Ikeda Kazuyuki , Tanaka Tamami , Kusuhara Koichi , Fujimoto Yukari , Fukase Koichi , Sueishi Katsuo , Hara Toshiro 
Published: February 2011

Objective—
The goal of this study was to investigate the effects of stimulants for a nucleotide-binding domain, leucine-rich repeat-containing (NLR) protein family on human artery endothelial cells and murine arteries.

Methods and Results—

Human coronary artery endothelial cells were challenged in vitro with microbial components that stimulate NLRs or Toll-like receptors. We found stimulatory effects of NLR and Toll-like receptor ligands on the adhesion molecule expression and cytokine secretion by human coronary artery endothelial cells. On the basis of these results, we examined the in vivo effects of these ligands in mice. Among them, FK565, 1 of the nucleotide-binding oligomerization domain (Nod)-1 ligands induced strong site-specific inflammation in the aortic root. Furthermore, coronary arteritis/valvulitis developed after direct oral administration or ad libitum drinking of FK565. The degree of the respective vascular inflammation was associated with persistent high expression of proinflammatory chemokine/cytokine and matrix metallopeptidase (
Mmp
) genes in each tissue in vivo by microarray analysis.

Conclusion—
This is the first coronary arteritis animal model induced by oral administration of a pure synthetic Nod1 ligand. The present study has demonstrated an unexpected role of Nod1 in the development of site-specific vascular inflammation, especially coronary arteritis. These findings might lead to the clarification of the pathogenesis and pathophysiology of coronary artery disease in humans.
Syndecan-4 Deficiency Limits Neointimal Formation After Vascular Injury by Regulating Vascular Smooth Muscle Cell Proliferation and Vascular Progenitor Cell Mobilization
Authors: Ikesue Masahiro , Matsui Yutaka , Ohta Daichi , Danzaki Keiko , Ito Koyu , Kanayama Masashi , Kurotaki Daisuke , Morimoto Junko , Kojima Tetsuhito , Tsutsui Hiroyuki , Uede Toshimitsu 
Published: February 2011

Objective—
Syndecan-4 (Syn4) is a heparan sulfate proteoglycan and works as a coreceptor for various growth factors. We examined whether Syn4 could be involved in the development of neointimal formation in vivo.

Methods and Results—

Wild-type (WT) and Syn4-deficient (Syn4
−/−
) mice were subjected to wire-induced femoral artery injury.
Syn4
mRNA was upregulated after vascular injury in WT mice. Neointimal formation was attenuated in Syn4
−/−
mice, concomitantly with the reduction of Ki67-positive vascular smooth muscle cells (VSMCs). Basic-fibroblast growth factor– or platelet-derived growth factor-BB–induced proliferation, extracellular signal-regulated kinase activation, and expression of cyclin D1 and Bcl-2 were impaired in VSMCs from Syn4
−/−
mice. To examine the role of Syn4 in bone marrow (BM)–derived vascular progenitor cells (VPCs) and vascular walls, we generated chimeric mice by replacing the BM cells of WT and Syn4
−/−
mice with those of WT or Syn4
−/−
mice. Syn4 expressed by both vascular walls and VPCs contributed to the neointimal formation after vascular injury. Although the numbers of VPCs were compatible between WT and Syn4
−/−
mice, mobilization of VPCs from BM after vascular injury was defective in Syn4
−/−
mice.

Conclusion—
Syn4 deficiency limits neointimal formation after vascular injury by regulating VSMC proliferation and VPC mobilization. Therefore, Syn4 may be a novel therapeutic target for preventing arterial restenosis after angioplasty.
Soluble Jagged-1 Inhibits Neointima Formation by Attenuating Notch-Herp2 Signaling
Authors: Caolo Vincenza , Schulten Henny M. , Zhuang Zhen W. , Murakami Masahiro , Wagenaar Allard , Verbruggen Sanne , Molin Daniel G.M. , Post Mark J. 
Published: February 2011

Objective—
Notch has been implicated in neointima formation as reflected by increased Notch/Jagged expression on vascular injury and the promigratory effect of Notch signaling on smooth muscle cells. Soluble Jagged-1 (sJag1) has been shown to inhibit Notch signaling in vitro; however, its capacity to suppress neointima formation remains unknown.

Methods and Results—
Balloon injury of rat carotid arteries induced Notch1, Notch3, and Jagged-1 expression at days 3 and 14 postinjury. Notch signaling was activated as shown by increased expression of the Notch target gene Herp2. Adenoviral sJag1 (Ad-sJag1) transfection reduced neointima formation in carotid artery and enhanced reendothelialization, whereas adenoviral full-length Jagged-1 (Ad-Fl-Jag1) or LacZ had no effect. Injury-induced Herp2 expression was absent in vessels treated with Ad-sJag1. Consistently, Herp2 expression was reduced in Ad-sJag1-infected or recombinant sJag1 –treated coronary artery smooth muscle cells (CASMCs). Ad-sJag1 had no effect on human umbilical endothelial cell behavior, but it significantly reduced proliferation and migration of CASMCs. Overexpression of Herp2 in sJag1-treated CASMCs rescued the migratory and proliferative capacity in vitro.

Conclusion—
Our results demonstrate that sJag1 can inhibit neointima formation after balloon injury by decreasing smooth muscle cell proliferation and migration through interference with Notch-Herp2 signaling.
Mean Platelet Volume May Represent a Predictive Parameter for Overall Vascular Mortality and Ischemic Heart Disease
Authors: Slavka Georg , Perkmann Thomas , Haslacher Helmuth , Greisenegger Stefan , Marsik Claudia , Wagner Oswald F. , Endler Georg 
Published: February 2011

Objective—
An increased mean platelet volume (MPV), as an indicator of larger, more reactive platelets resulting from an increased platelet turnover, may represent a risk factor for overall vascular mortality, including myocardial infarction. We intended to identify patients at higher risk of dying from vascular disease in a large, hospital-based cohort.

Methods and Results—
A total of 206 554 first-ever admissions to the Allgemeines Krankenhaus Wien for determination of MPV between January 1996 and July 2003 were included. Primary end points were overall vascular mortality and death due to ischemic heart disease. Multivariate Cox regression adjusted for sex, age, and platelet count was applied for analysis. MPV values were categorized into quintiles, with the lowest quintile serving as the reference category. Compared with individuals with lower MPV (<8.7 fL), hazard ratios for overall vascular mortality gradually increased to 1.5 in the highest category (≥11.01 fL). The relationship of MPV to ischemic heart disease was even stronger and increased from 1.2 (8.71 to 9.60 fL category) to 1.8 in the highest category (≥11.01 fL).

Conclusion—
Our results indicate that patients with an increased MPV (≥11.01 fL) are at higher risk of death due to ischemic heart disease, with hazard ratios comparable to those reported for obesity or smoking.
Toll-Like Receptor 4 Is Involved in Human and Mouse Vein Graft Remodeling, and Local Gene Silencing Reduces Vein Graft Disease in Hypercholesterolemic APOE*3Leiden Mice
Authors: Karper Jacco C. , de Vries Margreet R. , van den Brand Ben T. , Hoefer Imo E. , Fischer Jens W. , Jukema J. Wouter , Niessen Hans W.M. , Quax Paul H.A. 
Published: February 2011

Objective—
The goal of this study was to explore the role of Toll-like receptor 4 (TLR4) in vein graft remodeling and disease.

Methods and Results—

First, expression of TLR4 was analyzed in freshly isolated human saphenous veins (huSV), in freshly isolated huSV ex vivo perfused in an extracorporeal circulation, or in huSV used as coronary vein grafts. Marked induction of focal TLR4 expression was observed in perfused fresh huSV. Moreover, TLR4 was abundantly present in lesions in fresh huSV or in intimal hyperplasia in coronary vein grafts. Second, mouse venous bypass grafting was performed. In grafts of hypercholesterolemic APOE*3Leiden mice, increased TLR4 mRNA and protein was detected over time by reverse transcription–polymerase chain reaction and immunohistochemistry. Furthermore, the local presence of the endogenous TLR4 ligands heat shock protein 60, high-mobility group box 1, tenascin-C, and biglycan in the grafts was demonstrated. TLR4 deficiency in C3H-

Tlr4
LPS-d

(LPS indicates lipopolysaccharide) mice resulted in 48±12% less vein graft wall thickening (
P
=0.04) than in Balb/c controls. Moreover, local TLR4 gene silencing in hypercholesterolemic APOE*3Leiden mice using lentiviral short hairpin RNA against TLR4 administered perivascularly around vein grafts led to a 44±13% reduction of vessel wall thickening compared with controls (
P
=0.0059).

Conclusion—
These results indicate that TLR4 is involved in vein graft remodeling and can be used as a local therapeutic target against vein graft disease.
Increased Risk of Hemorrhagic Transformation in Ischemic Stroke Occurring During Warfarin Anticoagulation
Authors: Pfeilschifter Waltraud , Spitzer Daniel , Czech-Zechmeister Bożena , Steinmetz Helmuth , Foerch Christian 
Published: February 2011

Background and Purpose—
The prevalence of long-term oral anticoagulant therapy is rising. Treatment options for patients who have an ischemic stroke under oral anticoagulant therapy are limited, and clinical data on the risk of hemorrhagic transformation (HT) in this condition are scarce. We therefore aimed to establish a mouse model of ischemic stroke occurring during oral anticoagulant therapy to assess the frequency and characteristics of HT.

Methods—
C57BL/6 mice (n=59) were pretreated with warfarin. Untreated mice (n=32) served as controls. We performed a 3-hour transient filament occlusion of the right middle cerebral artery. In a first set of animals, ischemic lesion size and HT were evaluated macroscopically at 24 hours after middle cerebral artery occlusion. In a second set of mice, quantitative analysis of HT was performed at different time points after middle cerebral artery occlusion and in animals with different international normalized ratio levels using a photometric hemoglobin assay.

Results—

Oral anticoagulant therapy at the onset of ischemia led to HT in all anticoagulated mice, whereas only 14% of the control mice showed HT. Mean HT blood volume 24 hours after middle cerebral artery occlusion was 0.3±0.4 μL in controls, 4.2±1.7 μL in mice anticoagulated to a mean international normalized ratio of 1.9±0.5 (
P
<0.05 versus controls), and 5.2±2.7 μL in mice with an international normalized ratio of 2.9±0.9 (
P
<0.001 versus controls). Anticoagulated mice euthanized at the time point of reperfusion had less HT than mice euthanized after 21 hours of reperfusion (1.6±0.5 μL versus 5.9±3.6 μL,
P
<0.05).

Conclusions—
We present a mouse model of ischemic stroke occurring during oral anticoagulant therapy. Warfarin pretreatment dramatically increases the risk of HT 24 hours after middle cerebral artery occlusion. Reperfusion injury seems to be a critical component in this condition.