bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of combined antioxidant (β‐carotene, α‐tocopherol and ascorbic acid) supplementation on antioxidant capacity, DNA single‐strand breaks and levels of insulin‐like growth factor‐1/IGF‐binding protein 3 in the ferret model of lung cancer
Authors: Kim Yuri , Lian Fuzhi , Yeum Kyung‐Jin , Chongviriyaphan Nalinee , Choi Sang‐Woon , Russell Robert M. , Wang Xiang‐Dong 
Published: February 2007

AbstractInsulin‐like growth factor 1 (IGF‐1) and its major binding protein, IGF binding protein 3 (IGFBP‐3) are implicated in lung cancer and other malignancies. We have previously shown that the combination of three major antioxidants [β‐carotene (BC), α‐tocopherol (AT) and ascorbic acid (AA)] can prevent lung carcinogenesis in a 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone (NNK)‐treated and smoke‐exposed (SM) ferret model, which is highly analogous to humans. The present study is aimed at determining the effect of the combination of BC, AT and AA on antioxidant capacity, lymphocyte DNA damage, plasma IGF‐1 and IGFBP‐3 concentrations, as well as on IGF‐1/IGFBP‐3 mRNA expression in the tissues (lung and liver) of the ferrets. Ferrets were treated with or without combined antioxidant (BC, AT and AA) supplementation (AOX) for 6 months in the following 4 groups: (i) control; (ii) SM+NNK; (iii) AOX; and (iv) SM+NNK+AOX. Combined AOX supplementation significantly attenuated SM+NNK induced lymphocyte DNA damage in the ferret, while increasing resistance to oxidative damage when challenged with H2O2 in vitro. Ferrets treated with SM+NNK had significantly lower IGFBP‐3 mRNA expression in lungs, whereas there was significantly higher IGFBP‐3 mRNA expression in the liver, as well as higher circulating IGFBP‐3 concentrations. Combined AOX supplementation did not affect the plasma or tissue (lung and liver) ratio of IGF‐1/IGFBP‐3. Combined antioxidant supplementation provides protection against smoke‐induced oxidative DNA damage, but does not affect the IGF‐1/IGFBP‐3 system. Differential expression of IGFBP‐3 in different tissues indicates that caution should be taken when using plasma IGFBP‐3 as a biomarker of tissue status. © 2007 Wiley‐Liss, Inc.
Maternal smoking and the epidemic of testicular cancer—A nested case–control study
Authors: Pettersson Andreas , Akre Olof , Richiardi Lorenzo , Ekbom Anders , Kaijser Magnus 
Published: February 2007

AbstractFor no apparent reason, the incidence of testicular cancer has increased to epidemic proportions in many countries. Pregnancy smoking has been suggested to be a cause. Previous analytical studies have been negative, but the inherent difficulties in retrospective assessment of this exposure have led to no definite conclusion. We have conducted a population‐based case–control study on 192 cases of testicular germ‐cell cancer—born in Sweden in 1973 onwards and aged ≥15 at cancer diagnosis—and 494 matched controls, where data on maternal smoking were collected during pregnancy. We found no association with testicular cancer for maternal smoking during pregnancy (OR, 0.91; 95% CI, 0.64–1.30), and there was no evidence of a dose–response effect. We conclude that the epidemic rise in testicular cancer in many populations is not due to the surge in smoking among women. © 2007 Wiley‐Liss, Inc.
Cigarette smoke components inhibited intercellular communication and differentiation in human pancreatic ductal epithelial cells
Authors: Tai Mei‐Hui , Upham Brad L. , Olson Lawrence Karl , Tsao Ming‐Sound , Reed Donald N. , Trosko James E. 
Published: February 2007

AbstractSmoking is a well‐documented risk factor for the development of pancreatic adenocarcinoma. Although the most abundant polycyclic aromatic hydrocarbons (PAHs) in cigarette smoke are methylated anthracenes and phenanthrenes, the epigenetic toxicity of these compounds has not been extensively studied. We previously showed that methylanthracenes, which possess a bay‐like structure, affect epigenetic events such as an induced release of arachidonic acid, inhibition of gap junctional intercellular communication (GJIC) and induction of mitogen‐activated protein kinases in a pluripotent rat liver epithelial stem cell line. Anthracenes with no bay‐like structures were inactive. These biological effects are all molecular events associated with the promotional phase of cancer. A human immortalized, nontumorigenic pancreatic ductal epithelial cell line, H6c7, was examined to study the epigenetic toxicity of PAHs related to pancreatic cancer by using scrape‐loading dye transfer, immunostaining, RT‐PCR and telomerase assay methods. H6c7 cells were GJIC‐incompetent and exhibited high telomerase activity when grown in growth factor and hormone‐supplemented medium. In the presence of the cAMP elevating drugs (forskolin and IBMX) the cells became GJIC competent and expressed connexins. Telomerase activity was also decreased by cAMP elevating drug treatment. After induction of cAMP, 1‐methylanthracene with bay‐like structures inhibited GJIC, whereas the 2‐methylanthracene lacking a bay‐like structure had no effect on GJIC. Telomerase activity remained high in 1‐methylanthracene treatment but not with 2‐methylanthracene. These results indicate that a prominent component of cigarette smoke, namely methylanthracenes with distinct structural configurations, could be a potential etiological agent contributing to the epigenetic events of pancreatic cancer. © 2007 Wiley‐Liss, Inc.
Human papillomavirus‐16 DNA methylation patterns support a causal association of the virus with oral squamous cell carcinomas
Authors: Balderas‐Loaeza Adriana , Anaya‐Saavedra Gabriela , Ramirez‐Amador Velia A. , Guido‐Jimenez Miriam C. , Kalantari Mina , Calleja‐Macias Itzel E. , Bernard Hans‐Ulrich , Garcia‐Carranca Alejandro 
Published: February 2007

AbstractInfection with human papillomavirus‐16 (HPV‐16) is the cause of most anogenital carcinomas. This virus is also detected in about 20% of all head and neck squamous cell carcinomas. While there is strong evidence for a causal etiological role in the case of tonsillar carcinomas, causal association with malignant lesions of the oral cavity is not yet conclusive. Our previous investigations of HPV‐16 DNA methylation in anogenital sites have identified hypermethylation of the L1 gene and part of the long control region in many malignant lesions, but rarely in asymptomatic infections and low‐grade precancerous lesions. Here, we report hypermethylation of this diagnostically important segment of the viral DNA in 10 out of 12 HPV‐16 positive oral carcinomas from Mexican patients. These data indicate epigenetic changes of HPV‐16 in oral carcinomas similar to those in anogenital carcinomas, suggesting carcinogenic processes under the influence of HPV‐16 in most if not all of these oral malignant lesions. © 2007 Wiley‐Liss, Inc.
Identification of a novel single nucleotide polymorphism in the first tandem repeat sequence of the thymidylate synthase 2R allele
Authors: Lincz Lisa F. , Scorgie Fiona E. , Garg Madhu B. , Ackland Stephen P. 
Published: February 2007

AbstractThymidylate synthase (TS) activity is an important determinant of response to chemotherapy with fluoropyrimidine prodrugs and its expression is largely determined by the number of functional upstream stimulatory factor (USF) E‐box consensus elements present in the 5′regulatory region of the TYMS gene. Two known polymorphisms in this area, a variable number of tandem repeat (VNTR) consisting of 2 or 3 repeats (2R/3R) of a 28‐bp sequence and a further G > C single nucleotide substitution within the second repeat of the 3R, result in genotypes with between 2 and 4 functional repeats in most humans. Here, we identify a further G > C SNP in the first repeat of the TYMS 2R allele, which effectively abolishes the only functional USF protein binding site in this promoter. The frequency of the new allele was found to be 4.2% (95% CI = 1.4–9.6%), accounting for 8.8% (95% CI = 2.9–19.3%) of all 2R alleles in our patient cohort. Thus, we observed that the lowest number of inherited functional binding sites is 1 instead of 2 as previously thought, and could potentially be 0 in a homozygous individual. This would severely decrease TS expression and may have implications for predicting efficacy and toxicity of therapy with commonly used fluorouracil‐based therapy regimes. © 2007 Wiley‐Liss, Inc.
Smoking and survival after breast cancer diagnosis
Authors: Holmes Michelle D. , Murin Susan , Chen Wendy Y. , Kroenke Candyce H. , Spiegelman Donna , Colditz Graham A. 
Published: February 2007

AbstractWe examined whether a history of smoking is associated with an increased risk of death from any cause or from breast cancer, among women diagnosed with breast cancer. This was a prospective observational study among 5,056 women from the Nurses' Health Study with Stages I–III invasive breast cancer diagnosed between 1978 and 2002 and for whom we had information on smoking, and who were followed until January 2002 or death, whichever came first. Subjects were classified as current, former or never smokers based upon smoking status at the biennial questionnaire immediately preceding the breast cancer diagnosis. In multivariate‐adjusted analyses, compared with never smokers, women who were current smokers had a 43% increased adjusted relative risk (RR) [95% confidence interval (95% CI): 1.24–1.65] of death from any cause. A strong linear gradient was observed with the number of cigarettes per day smoked, p‐trend <0.0001; the RR (95% CI) for 1–14, 15–24 and 25 or more cigarettes per day was 1.27 (1.01–1.61), 1.30 (1.08–1.57) and 1.79 (1.47–2.19). In contrast, there was no association with current smoking and breast cancer death; the RR (95% CI) was 1.00 (0.83–1.19). Current and past smokers were more likely than never smokers to die from primary lung cancer, chronic obstructive pulmonary disease and other lung diseases. We conclude that a history of smoking increased mortality following diagnosis with breast cancer, but did not increase mortality from breast cancer. © 2007 Wiley‐Liss, Inc.
In vitro oxime reactivation of red blood cell acetylcholinesterase inhibited by methyl‐paraoxon
Authors: Petroianu G. A. , Arafat K. , Nurulain S. M. , Kuča K. , Kassa J. 
Published: February 2007

AbstractOximes are cholinesterase reactivators of use in poisoning with organophosphorus ester enzyme inhibitors. Pralidoxime (PRX) is the oxime used in the United States. Clinical experience with pralidoxime (and other oximes) is disappointing and the routine use has been questioned. Furthermore oximes are not equally effective against all existent enzyme inhibitors. There is a clear demand for ‘broad spectrum’ cholinesterase reactivators with a higher efficacy than those clinically available. To meet this need over the years new reactivators of cholinesterase of potential clinical utility have been developed.The purpose of the study was to quantify ‘in vitro’ the extent of protection conferred by available (pralidoxime and methoxime) and experimental (K‐27, K‐33 and K‐48) oximes, using methyl‐paraoxon (methyl‐POX) as an esterase inhibitor and to compare the results with those previously obtained using paraoxon (POX) as an inhibitor.Red blood cell (RBC) acetylcholinesterase (AChE) activities in whole blood were measured photometrically in the presence of different methyl‐POX concentrations and IC50 values calculated. Determinations were repeated in the presence of increasing oxime concentrations. The IC50 of methyl‐POX (59 nm) increased with the oxime concentration in a linear manner. The calculated IC50 values were plotted against the oxime concentrations to obtain an IC50 shift curve. The slope of the shift curve (tg α) was used to quantify the magnitude of the protective effect (nm IC50 increase per µm reactivator).Based on our determinations the new K‐series of reactivators is superior to pralidoxime (tg α = 1.9) and methoxime (tg α = 0.7), K‐27 and K‐48 being the outstanding compounds with a tg α value of 10 (nm IC50 increase per µm reactivator), which is ≈ five times the reactivator ability of PRX. The tg α value determined for K‐33 was 6.3.The ranking of reactivator potencies of the examined oximes determined with methyl‐POX as an inhibitor (K‐27 = K‐48 > K‐33 > pralidoxime > methoxime) is similar to the ranking previously reported by us using POX as an inhibitor (K‐27 ≥ K‐48 > K‐33 > methoxime = pralidoxime). There is an (expected) inverse relationship between the binding constant K and the slope of the IC50 shift curve (tg α) for all oximes examined. K‐27 and K‐48 (the most protective substances judging by the tg α) having the lowest K value (highest affinity).In vivo testing of the new oximes as methyl‐paraoxon protective agents is necessary. Copyright © 2007 John Wiley & Sons, Ltd.
Enhanced bone bonding of hydroxyapatite‐coated titanium implants by electrical polarization
Authors: Kobayashi Takayuki , Itoh Soichiro , Nakamura Satoshi , Nakamura Miho , Shinomiya Kenichi , Yamashita Kimihiro 
Published: February 2007

AbstractHydroxyapatite (HAp) coatings are applied to orthopedic and dental implants made of titanium (Ti) and its alloys in order to increase their bioactivities and to offset the mechanical weakness of HAp. We examined thein vivoeffects of electrical polarization on the bone bonding of HAp‐coated Ti. Polarized samples with a negatively or positively charged HAp‐coated surface (N‐ or P‐surface, respectively) were randomly implanted in the femora and tibiae of canines. As controls, nonpolarized HAp‐coated Ti substrates with 0‐surfaces were implanted. Direct bonding between the newly formed bone and HAp‐coated Ti was observed with the O‐, N‐, and P‐surfaces. The results of a pullout test were consistent with the amount of newly formed bone bonded directly to the surface of HAp‐coated Ti. Electrically polarized HAp‐coated Ti substrates, especially those with N‐surfaces, exposed to recipient bone enhance bone bonding and could enable earlier weight‐bearing loads after operations. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Expression of core binding factor 1 and osteoblastic markers in C2C12 cells induced by calcium phosphate ceramics in vitro
Authors: Tan Yanfei , Wang Gang , Fan Hongsong , Wang Xinlong , Lu Jian , Zhang Xingdong 
Published: February 2007

AbstractThe in vivo osteoinductive capacity of porous calcium phosphate ceramics (Ca/P ceramics) with special structure and phase composition had been found for almost decades. The mechanism of the osteoinductivity of porous calcium phosphate is studied by C2C12 cells culture in this paper. C2C12 cells were cocultured with four kinds of porous Ca/P ceramics for 2 and 5 days, without adding other growth factors. The four kinds of Ca/P ceramics were pure HA sintered at 1250°C and HA/TCP with a ratio of 60/40 sintered at 1100, 1200, and 1250°C respectively. RT‐PCR analysis found that the Ca/P ceramics induced the expression of Cbfa1, collagen type I, bone sialoprotein, and osteocalcin in C2C12 cells, while they did not induce mRNA expression of Indian hedgehog (IHH) that regulate chondrocyte differentiation. Our results showed that Ca/P ceramics alone were sufficient to induce C2C12 cells differentiation. The induction of bone‐related markers expression by Ca/P ceramics in osteoprogenitor cells suggested that the osteogenesis induced by the ceramics was intramembranous and the osteoinductivity was their intrinsic property. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
In vitro culture of mesenchymal cells onto nanocrystalline hydroxyapatite‐coated Ti13Nb13Zr alloy
Authors: Bigi A. , Nicoli‐Aldini N. , Bracci B. , Zavan B. , Boanini E. , Sbaiz F. , Panzavolta S. , Zorzato G. , Giardino R. , Facchini A. , Abatangelo G. , Cortivo R. 
Published: February 2007

AbstractIn this study we coated a new biocompatible, nanostructured titanium alloy, Ti13Nb13Zr, with a thin layer of hydroxyapatite nanocrystals and we investigated the response of human bone‐marrow‐derived mesenchymal cells. The coating was realized using a slightly supersaturated CaP solution, which provokes a fast deposition of nanocrystalline hydroxyapatite. A thin layer of deposition is appreciable on the etched Ti13Nb13Zr substrates after just 1.5 h soaking in the CaP solution, and it reaches a thickness of 1–2 μm after 3 h soaking. The coating seems thinner than that deposited on Ti6Al4V, which was examined for comparison, likely because of the different roughness profiles of the two etched alloys, and it is constituted of elongated HA nanocrystals, with a mean length of about 100 nm. Mesenchymal stem cells were seeded onto coated and uncoated Ti alloys and cultured for up to 35 days. Cell morphology, proliferation and differentiation were evaluated. The cells display good adhesion and proliferation on the uncoated substrates, whereas the presence of hydroxyapatite coating slightly reduces cell proliferation and induces differentiation of MSCs towards a phenotypic osteoblastic lineage, in agreement with the increase of the expression of osteopontin, osteonectin and collagen type I, evaluated by means of rt‐PCR. Type I collagen expression is higher in Ti13Nb13Zr MSC culture compared to Ti6Al4V, standing for a more efficient extracellular matrix deposition. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Effects of mannosylated glycopolymers on specific interaction to bone marrow hematopoietic and progenitor cells derived from murine species
Authors: Park Keun‐Hong , Na Kun , Lee Yong Su , Chang Won‐Kyong , Park Jin‐Ki , Akaike Thoshihiro , Kim Dong Ku 
Published: February 2007

AbstractPoly[N‐pvinylbenzyl‐O‐D‐galactopyranosyl‐(1‐4)‐D‐glucoamide], poly[N‐pvinylbenzyl‐O‐D‐glucopyranosyl‐(1‐4)‐D‐glucoamide], and poly[N‐p‐vinylbenzyl‐O‐mannopyranosyl‐(1‐4)‐D‐gluconamide] (referred to as PVLA, PVMA, and PV‐Man) are polystyrene derivatives that contain galactose, glucose, and mannose moieties, which interact with hematopoietic cells (HCs). To clarify the specific interaction between the glucopolymers and hematopoietic cells, glycopolymers labeled with fluorescent isothiocyanate (FITC) were used to follow the specific interaction, which was visualized by confocal laser microscopy. We found that PV‐Man binds strongly to HCs, probably because of a specific interaction mediated by specific receptors present on the cell membrane, while some cytotoxicity when was observed when PV‐Man interacted with the cell membrane. The fluorescence intensity between PV‐Man and HCs was up to four‐fold (0.14 ± 0.04) that of PVMA and PVLA with hematopoietic HCs (0.033 ± 0.01). Moreover, cellular fluorescence increased significantly with increasing incubation time and increasing polymer concentration. Using hematopoietic lineage‐specific antibodies, cells were stained and analyzed by flow cytometry to confirm which HCs showed specific binding with glycopolymers, especially hematopoietic stem cells and progenitor cells (c‐kit+), B‐lymphocyte progenitor cells (B220+), monocyte cells (CD11b+), and erythrocytes (Ter119+). © 2007 Wiley Periodicals, Inc. J Biomed Mater Res 2007
Preparation and bioactive characteristics of a porous 13–93 glass, and fabrication into the articulating surface of a proximal tibia
Authors: Fu Qiang , Rahaman Mohamed N. , Bal B. Sonny , Huang Wenhai , Day Delbert E. 
Published: February 2007

AbstractThe silicate‐based 45S5 bioactive glass, typically in particulate form, has been widely investigated for bone repair. However, its application as a scaffold for bone tissue engineering is limited due to the difficulty of forming porous three‐dimensional constructs with complex shapes. In this study, the use of another silicate‐based bioactive glass, referred to as 13–93, was investigated for the preparation of porous constructs. Particles of 13–93 glass (255–325 μm) were consolidated and sintered to form cylindrical constructs. Characterization of these constructs was performed using mercury porosimetry, scanning electron microscopy (SEM), and mechanical testing. Constructs with porosities of 40–45% and pore sizes in the range 100–300 μm were found to have a compressive strength of 22 ± 1 MPa. The bioactivity of the 13–93 glass was studied by immersing disks in a simulated body fluid at 37°C and characterizing the reaction products. X‐ray diffraction, Fourier transform infrared (FTIR) spectroscopy, and SEM showed the formation of a crystalline hydroxyapatite layer on the glass surface after ∼7 days. The ability to fabricate the complex geometrical shape of the articulating surface of a human tibia from 13–93 glass particles was demonstrated. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Long‐term activation of adenosine monophosphate‐activated protein kinase attenuates pressure‐overload‐induced cardiac hypertrophy
Authors: Li Hong‐Liang , Yin Ran , Chen Dandan , Liu Dan , Wang Dong , Yang Qinglin , Dong Yu‐Gang 
Published: February 2007

AbstractRecent in vitro studies suggest that adenosine monophosphate (AMP)‐activated protein kinase (AMPK) exerts inhibitory effects on cardiac hypertrophy. However, it is unclear whether long‐term activation of AMPK will affect cardiac hypertrophy in vivo. In these reports, we investigate the in vivo effects of long‐term AMPK activation on cardiac hypertrophy and the related molecular mechanisms. To examine the effects of AMPK activation in the development of pressure overload‐induced cardiac hypertrophy, we administered 5‐aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks. We found that long‐term AMPK activation attenuated cardiac hypertrophy, and improved cardiac function in rats subjected to TAC. Furthermore, long‐term AMPK activation attenuated protein synthesis, diminished calcineurin‐nuclear factor of activated T cells (NFAT) and nuclear factor κB (NF‐κB) signaling in pressure overload‐induced hypertrophic hearts. Our in vitro experiments further proved that activation of AMPK by infection of AdAMPK blocked cardiac hypertrophy and NFAT, NF‐κB, and MAPK signal pathways. The present study demonstrates for the first time that pharmacological activation of AMPK inhibits cardiac hypertrophy in through blocking signaling transduction pathways that are involved in cardiac growth. It presents a potential therapy strategy to inhibit pathological cardiac hypertrophy by increasing the activity of AMPK. J. Cell. Biochem. 100: 1086–1099, 2007. © 2007 Wiley‐Liss, Inc.
Effect of different treatments of long‐range interactions and sampling conditions in molecular dynamic simulations of rhodopsin embedded in a dipalmitoyl phosphatidylcholine bilayer
Authors: Cordomí Arnau , Edholm Olle , Perez Juan J. 
Published: February 2007

AbstractThe present study analyzes the effect of the simulation conditions on the results of molecular dynamics simulations of G‐protein coupled receptors (GPCRs) performed with an explicit lipid bilayer. Accordingly, the present work reports the analysis of different simulations of bovine rhodopsin embedded in a dipalmitoyl phosphatidylcholine (DPPC) lipid bilayer using two different sampling conditions and two different approaches for the treatment of long‐range electrostatic interactions. Specifically, sampling was carried out either by using the statistical ensembles NVT or NPT (constant number of atoms, a pressure of 1 atm in all directions and fixed temperature), and the electrostatic interactions were treated either by using a twin‐cutoff, or the particle mesh Ewald summation method (PME). The results of the present study suggest that the use of the NPT ensemble in combination with the PME method provide more realistic simulations. The use of NPT during the equilibration avoids the need of an a priori estimation of the box dimensions, giving the correct area per lipid. However, once the system is equilibrated, the simulations are irrespective of the sampling conditions used. The use of an electrostatic cutoff induces artifacts on both lipid thickness and the ion distribution, but has no direct effect on the protein and water molecules. © 2007 Wiley Periodicals, Inc. J Comput Chem, 2007