bluuebunny/crossref_metadata_2025_split huggingface dataset:
Leaching and mechanical properties characterization of dental composites
Authors: Drummond James L. , Andronova Ksenia , Al‐Turki Lulwa I. , Slaughter Leslee D. 
Published: June 2004

AbstractThe objective of this study was to determine the leaching of Ba, Si, and Sr from four dental composites: Restolux (RX), Micronew (M), Renew (RW), and Choice (C) and to correlate the effects of such leaching with flexure strength and modulus of elasticity. The specimens were 3 × 3 × 25‐mm bars, polished with 120‐ and 240‐grit SiC paper, and were aged for 4, 6, and 8 months in artificial saliva, distilled water, and a 50/50 mixture of ethanol and distilled water. Inductively coupled plasma with mass spectroscopy (ICP/MS) was used to determine the ion concentrations after aging. The greatest release of Ba and Sr occurred after aging in 50/50 volume fraction mixture of ethanol/water and for Si in artificial saliva. The 50/50 solution caused a breakdown of the resin and glass matrix, resulting in an increase of Ba and Sr, whereas aging in artificial saliva resulted in an ion charge balance, which allowed an elevated and continuous release of Si. The flexure strength and the elastic modulus showed a gradual decrease over time, with the greatest decreases occurring following aging in the 50/50 water/ethanol solution, but little correlation with the leaching of the filler ions. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 71B: 172–180, 2004
Bisphenol A from dental polycarbonate crown upregulates the expression of hTERT
Authors: Takahashi Akiko , Higashino Fumihiro , Aoyagi Mariko , Kyo Satoru , Nakata Takashi , Noda Mamoru , Shindoh Masanobu , Kohgo Takao , Sano Hidehiko 
Published: June 2004

AbstractBisphenol A (BPA) is one of the endocrine‐disrupting chemicals (EDCs) that possess estrogen‐like biologic activity. Many dental materials have been reported to release BPA. However, there are few reports available on the release of BPA from dental polycarbonates. The purpose of this study was to investigate the release of BPA from dental polycarbonate crowns and to evaluate the estrogenic activity of BPA. Polycarbonate crowns were immersed in five solvents (water, ethanol, n‐hepthane, acetic acid, and acetonitrile) at 37 or 65°C for 24 h. The elution from the material was analyzed by high‐performance liquid‐chromatography (HPLC) and mass‐spectrometry (MS) analysis. BPA release was detected corresponding to the degradation of dental polycarbonates under the some storage conditions (ethanol, acetic acid, and acetonitrile). A previous report proved that estrogen increased human telomerase catalytic subunit (hTERT) mRNA, whereas the effect of EDCs on the hTERT promoter has never been reported. The estrogenic activity of BPA was analyzed by luciferase assay with the use of the hTERT promoter. This assay revealed that BPA was a positive regulator of hTERT transcription. In addition, quantitative real‐time PCR analysis showed that BPA increased the expression level of hTERT mRNA in MCF7 cells. Herein, it is demonstrated that hTERT is a new target of BPA. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 71B: 214–221, 2004
Prolonged cytotoxic effect of colchicine released from biodegradable microspheres
Authors: Muvaffak Asli , Gurhan Ismet , Hasirci Nesrin 
Published: June 2004

AbstractOne the main problems of cancer chemotherapy is the unwanted damage to normal cells caused by the high toxicities of anticancer drugs. Any system of controlled drug delivery that would reduce the total amount of drug required, and thus reduce the side effects, would potentially help to improve chemotherapy. In this respect, biodegradable gelatin microspheres were prepared by water/oil emulsion polymerization and by crosslinking with glutaraldehyde (GTA) as the drug‐carrier system. Microspheres were loaded with colchicine, a model antimitotic drug, which was frequently used as an antimitotic agent in cancer research involving cell cultures. Microsphere sizes, swelling and degradation properties, drug‐release kinetics, and cytotoxities were studied. Swelling characteristics of microspheres changed upon changing GTA concentration. A decrease in swelling values was recorded as GTA crosslink density was increased.In vitrodrug release in PBS (0.01M, pH 7.4) showed rapid colchicine release up to ∼83% (att= 92 h) for microspheres with low GTA (0.05% v/v), whereas a slower release profile (only ∼39%) was obtained for microspheres with high GTA (0.50% v/v) content, for the same period. Cytotoxicity tests with MCF‐7, HeLa and H‐82 cancer cell lines showed that free colchicine was very toxic, showing an ∼100% lethal effect in both HeLa and H‐82 cell lines and more than 50% decrease in viability in MCF‐7 cells in 4 days. Indeed, entrapped colchicine indicated similar initial high toxic effect on cell viability in MCF‐7 cell line and this effect became more dominant as colchicine continued to be released from microspheres in the same period. In conclusion, the control of the release rate of colchicine from gelatin microspheres was achieved underin vitroconditions by gelatin through the alteration of crosslinking conditions. Indeed, the results suggested the potential application of gelatin microspheres crosslinked with GTA as a sustained drug‐delivery system for anticancer drugs for local chemotherapy administrations. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 71B: 295–304, 2004
Evaluation of hot‐pressed hydroxyapatite/poly‐L‐lactide composite biomaterial characteristics
Authors: Ignjatovic Nenad , Suljovrujic Edin , Budinski‐Simendic Jaroslava , Krakovsky Ivan , Uskokovic Dragan 
Published: June 2004

AbstractHydroxyapatite/poly‐L‐lactide (HAp/PLLA) is a ceramic/polymer composite, whose application as a resorbable biomaterial for the substitution and repair of hard bone tissue is widely promising in orthopedic, oral, maxillofacial, and reconstructive surgery. Hot processing is a necessary step for obtaining HAp/PLLA composite blocks with mechanical properties similar to those of bones. In this article, the changes in structure and physicochemical properties of HAp/PLLA composite, hot pressed for different pressing times (5, 15, 30, 45, and 60 min), were studied. Because the morphology of HAp/PLLA composite biomaterial is very sensitive to this procedure, its surface microstructure was analyzed by scanning electron microscopy (SEM) coupled with an energy‐dispersive X‐ray (EDX) detector system. Structural changes occurring in the material, mostly changes in crystallinity of PLLA, were studied by wide‐angle X‐ray structural analyses (WAXS) and infrared (FTIR) spectroscopy. Using differential scanning calorimetry (DSC), thermogravimetric analysis (TGA), and gel permeation chromatography (GPC), the influence of hot pressing on the properties, crystallization kinetics, and decomposition of HAp/PLLA composite biomaterial was analyzed. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 71B: 284–294, 2004
Analysis of mesenchymal cells derived from an chondrodysplasia punctuate patient and donors
Authors: Shur Irena , Reish Orit , Ezra Eli , Benayahu Dafna 
Published: June 2004

AbstractConradi–Hunermann syndrome (CDPX2) is X‐linked dominant disorder appeared with aberrant punctuate calcification. The skeletal cells derived from the marrow stroma are active in maintaining the skeletal formation. We obtained mesenchymal stem cells from a patient with CDPX2 and studied the formation of colony forming unit‐fibroblast (CFU‐F) in vitro in comparison cells obtained from normal donors. Cultured cells were studied morphologically and subjected to gene expression analysis. Marrow stromal cells (MSC)‐chondrodysplasia punctuate (CDP) cells from CDPX2 were identified by their mosaic morphology formed three phenotypically distinct types of CFU‐F colonies. One type consisted of normal fibroblasts with developed cell body and cellular processes; the second type contained pathological small cells without processes; and the third type comprised of mixed cells. We compared gene expression by the MSC‐CDP to cells from normal donors. Transcription factors analyzed proliferation potential were similar in both normal and mixed colonies of MSC‐CDP and similar to normal MSCs. The message expression for cytokines and extra cellular matrix (ECM) proteins revealed similar expression for biglycan, osteocalcin, and osteonectin, while IL‐6, IL‐11, and M‐CSF mRNA levels were significantly higher in normal cells than in MSC‐CDP. Mixed cells had elevated levels for IL‐6 and M‐CSF mRNA, but expressed IL‐11 at the normal range. The studied genes were expressed at lower levels by the pathological (MSC‐CDP) cells compared to normal ones. Hence, MSC‐CDP was demonstrated to display abnormal morphology and transcription of several investigated genes. This study further illuminates the basis of the mosaic pattern of mesenchymal cells derived from a patient affected with CDPX2, and their gene expression involvement. © 2004 Wiley‐Liss, Inc.
A3 adenosine receptor deficiency does not influence atherogenesis
Authors: Jones Matthew R. , Zhao Zhihui , Sullivan Christopher P. , Schreiber Barbara M. , Stone Phillip J. , Toselli Paul A. , Kagan Herbert M. , Cohen Richard A. , Ravid Katya 
Published: June 2004

AbstractAtherosclerosis is a multifactorial disease, the progression of which is modulated by several factors, including inflammation and hypercholesterolemia. The A3 adenosine receptor (A3AR) has been reported to affect mast cell degranulation leading to inflammation, as well as to influence cardiovascular homeostasis. Here, we show that its deletion can also impact vascular smooth muscle cell (VSMC) proliferation in vitro. Based on these observations, we hypothesized that A3AR deficiency would affect atheromatous lesion development in vivo. Our results indicate that the expression of the matrix enzyme lysyl oxidase (LO) is increased while the proliferation potential of VSMC is decreased in A3AR‐null aortas. This is in accordance with the previously reported inverse correlation between LO level and proliferation. Nevertheless, we found that A3‐deficiency does not protect vessels against atherogenesis. This was demonstrated in mouse models of high fat diet‐induced atherosclerosis and guidewire‐induced femoral artery injury. We conclude that the contributions of the A3AR to inflammation and to modulating LO levels are not significant enough to control vascular response to injury. © 2004 Wiley‐Liss, Inc.
Inhibition of phenylephrine‐induced cardiac hypertrophy by docosahexaenoic acid
Authors: Siddiqui Rafat A. , Shaikh Saame Raza , Kovacs Richard , Stillwell William , Zaloga Gary 
Published: June 2004

AbstractMany of the cardiovascular benefits of fish oil result from the antiarrhythmic actions of the n‐3 polyunsaturated lipids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). The beneficial effects of DHA/EPA in patients with coronary artery disease and myocardial infarction may also result from modulation of the myocardial hypertrophic response. Hypertrophy was assessed in neonatal cardiomyocytes exposed to phenylephrine (PE) by measuring cell surface area, total protein synthesis (14C leucine incorporation), and the organization of sarcomeric α‐actinin and by monitoring expression of atrial natriuretic factor (ANF). We report that PE induced a twofold increase in cell surface area and protein synthesis in cardiomyocytes. The hypertrophied cardiomyocytes also exhibited increased expression of ANF in perinuclear regions and organization of sarcomeric α‐actinin into classical z‐bands. Treatment of cardiomyocytes with 5 μM DHA effectively prevented PE‐induced hypertrophy as shown by inhibition of surface area expansion and protein synthesis, inhibition of ANF expression, and prevention of α‐actinin organization into z‐bands. DHA treatment prevented PE‐induced activation of Ras and Raf‐1 kinase. The upstream inhibition of Ras → Raf‐1 effectively prevented translocation and nuclear localization of phosphorylated extracellularly regulated kinase 1 and 2 (Erk1/2). These effects consequently led to inhibition of nuclear translocation, and hence, activation of the downstream signaling enzyme p90 ribosomal S6 kinase (p90rsk). These results indicate that PE‐induced cardiac hypertrophy can be minimized by DHA. Our results suggest that inhibition of Ras → Raf‐1 → Erk1/2 → p90rsk → hypertrophy is one possible pathway by which DHA can inhibit cardiac hypertrophy. In vivo studies are needed to confirm these in vitro effects of DHA. © 2004 Wiley‐Liss, Inc.
Mitochondrial P2Y‐Like receptors link cytosolic adenosine nucleotides to mitochondrial calcium uptake
Authors: Belous Andrey , Wakata Aya , Knox Clayton D. , Nicoud Ian B. , Pierce Janene , Anderson Christopher D. , Pinson C. Wright , Chari Ravi S. 
Published: June 2004

AbstractATP is a known extracellular ligand for cell membrane purinergic receptors. Intracellular ATP can work also as a regulatory ligand via binding sites on functional proteins. We report herein the existence of P2Y1‐like and P2Y2‐like receptors in hepatocyte mitochondria (mP2Y1 and mP2Y2), which regulate mCa2+ uptake though the uniporter. Mitochondrial P2Y1 activation stimulates mCa2+ uptake; whereas, mP2Y2 activation inhibits mCa2+ uptake. ATP acts preferentially on mP2Y2 receptors, while ADP and AMP‐PNP stimulate both the mP2Y1 and mP2Y2. PPADS inhibits ADP stimulated mP2Y1‐mediated mCa2+ uptake. In addition, UTP, a selective P2Y2 agonist, strongly inhibits mCa2+ uptake. The newly discovered presence and function of these receptors is significant because it explains increased mCa2+ uptake in the setting of low cytosolic [ATP] and, therefore, establishes a mechanism for direct feedback in which cytosolic [ATP] governs mitochondrial ATP production through regulation of mCa2+ uptake. © 2004 Wiley‐Liss, Inc.
Increased density of retinal pigment epithelium in cd81−/− mice
Authors: Song Bong K. , Levy Shoshana , Geisert Eldon E. 
Published: June 2004

AbstractOur laboratories have focused on the role of the tetraspanin CD81 in the regulation of mitotic activity. Previously we have shown that antibodies directed against CD81 can block the proliferation of cultured retinal pigment epithelial (RPE) cells. The present study investigates the role of this protein by analyzing the structure of the adult retina in mice with a null mutation of cd81. Adult cd81−/− mice were produced by crossing two inbred strains, NIHS‐BC/Tac and 129X1/SvJ, carrying the cd81 mutation as heterozygotes (+/−). Seven cd81−/− mice and 11 wildtype (cd81+/+) littermates were anesthetized and perfused with paraformaldehyde. The eyes were removed and processed for examination by light and electron microscopy. In general, the retinas of the cd81−/− mice appeared normal. However, upon close examination, there was an 18% increase in the number of RPE nuclei in the cd81−/− mice. The photoreceptor layer of the cd81−/− mice was significantly thinner than that of the wild‐type mice, even though there was no difference in the total thickness of the retinas in the two groups of mice. At the electron microscopic level we did not observe any differences in cell–cell junctions in the retinas of the cd81−/− mice as compared to their wild‐type littermates. These data support a role for CD81 controlling cell‐cycle and the number of RPE nuclei in the mouse retina. © 2004 Wiley‐Liss, Inc.
Radiation‐induced genomic instability: A role for secreted soluble factors in communicating the radiation response to non‐irradiated cells
Authors: Sowa Resat Marianne B. , Morgan William F. 
Published: June 2004

AbstractRadiation induced genomic instability can be described as the increased rate of genomic alterations occurring in the progeny of an irradiated cell. Its manifestations are the dynamic ongoing production of chromosomal rearrangements, mutations, gene amplifications, transformation, microsatellite instability, and/or cell killing. In this prospectus, we present the hypothesis that cellular exposure to ionizing radiation can result in the secretion of soluble factors by irradiated cells and/or their progeny, and that these factors can elicit responses in other cells thereby initiating and perpetuating ongoing genomic instability. © 2004 Wiley‐Liss, Inc.
In vitro and in vivo prevention of HIV protease inhibitor‐induced insulin resistance by a novel small molecule insulin receptor activator
Authors: Cheng Mingshan , Chen Seiyu , Schow Steven R. , Manchem Vara Prasad , Spevak Wayne R. , Cristobal Cristina P. , Shi Songyuan , Macsata Robert W. , Lum Robert T. , Goldfine Ira D. , Keck James G. 
Published: June 2004

AbstractProtease inhibitor (PI) therapy for the treatment of patients infected with human immunodeficiency virus is frequently associated with insulin resistance and diabetic complications. These adverse effects of PI treatment result to a large extent from their inhibition of insulin‐stimulated glucose transport. Insulin receptor (IR) activators that enhance the insulin signaling pathway could be effective in treating this resistance. However, there are no agents reported that reverse inhibition of insulin action by PIs. Herein, we describe the effects of TLK19781. This compound is a non‐peptide, small molecule, activator of the IR. We now report in cultured cells, made insulin resistant HIV by PI treatment, that TLK19781 both increased the content of insulin‐stimulated GLUT4 at the plasma membrane, and enhanced insulin‐stimulated glucose transport. In addition, oral administration of TLK19781 with the PI, indinavir improved glucose tolerance in rats made insulin resistant. These results suggest, therefore, that IR activators such as TLK19781 may be useful in treating the insulin resistance associated with PIs. © 2004 Wiley‐Liss, Inc.
Dual effect of heparin on cultured adult rat cardiomyocytes
Authors: Rezgui Nebil , Stefano Corda , Françoise Marotte , Jane‐Lise Samuel 
Published: June 2004

AbstractHeparin has been widely reported to inhibit the growth of several cell types including neonatal rat cardiac myocyte (NRCM) but its effect on adult rat ventricular myocyte (ARVM) is unknown. To determine whether heparin is able to modulate ARVM protein synthesis capacity and if so which pathway is involved in this response, ARVM were cultured in presence or absence of 5% human serum and exposed to heparin (2–2,000 μg/ml) or its analogue xylan (0.5 and 50 μg/ml), and either the Ca2+ chelator BAPTA/AM (10 μg/ml), or the calcineurin inhibitor FK506 (10 μg/ml), and heparinase I (0.1–10 U/ml) for 2 days. The protein synthesis (PS) was measured after 24 h incorporation of [14C]‐Phenylalanine in ARVM. Independently of the serum presence, heparin and xylan altered PS in a bimodal dose‐dependent manner. At high doses, heparin and xylan (2,000 and 50 μg/ml, respectively) either had no effect (without serum) or inhibited PS (with serum). In absence of serum, low doses of heparin or xylan (20 and 0.5 μg/ml, respectively) amplified the PS process in ARVM (2‐fold, P < 0.05). FK506 inhibited the trophic response to 20 μg/ml heparin alone (−39%, P < 0.05). In presence of serum, the heparin induced‐trophic effect, that was not significantly altered by FK506, was inhibited by BAPTA/AM (−32%, P < 0.05). Finally, heparinase I that increased PS in NRCM had no effect on ARVM growth. This study strongly suggests that heparin dose‐dependently modulated PS in ARVM, this result being not observed in neonatal cells. Different mechanisms involving intracellular Ca2+ play a role in the PS response of ARVM to low concentrations of heparin, the intracellular pathways depending on the presence of serum. © 2004 Wiley‐Liss, Inc.
Heme oxygenase‐1 protects against apoptosis induced by tumor necrosis factor‐α and cycloheximide in papillary thyroid carcinoma cells
Authors: Chen George G. , Liu Z.M. , Vlantis A.C. , Tse G.M.K. , Leung B.C.H. , van Hasselt C.A. 
Published: June 2004

AbstractHeme oxygenase‐1 (HO‐1) plays a role in the resistance to apoptosis of several types of cells, but its role in the development of thyroid cancer is unknown. In this study, we investigated the regulation of HO‐1 in human papillary thyroid carcinoma cells (KAT5). The results show that HO‐1 is significantly induced by hemin and cadmium. In addition to inducing HO‐1, hemin and cadmium also cause a rise in the levels of p21, a cyclin‐dependent kinase inhibitor. Cells with increased levels of HO‐1 and p21 were more resistant to apoptotic stimuli than cells with normal levels. The cells resistant to apoptosis also displayed an increased arrest at the G0/G1 phase of the cell‐cycle. The induced levels of HO‐1 and p21 were significantly reduced by p38 mitogen‐activated protein kinase (p38 MAPK) and extracellular‐regulated kinase (ERK) inhibitors. More importantly, KAT5 cells regained their sensitivity to apoptotic stimuli after they were treated with these kinase inhibitors, indicating that p38 MAPK and ERK are required for the resistance to apoptosis conferred by HO‐1. Furthermore, we demonstrated that increased levels of HO‐1 and p21 expression are associated with an increase in the activity of NF‐kappaB and that inhibiting NF‐kappaB leads to a block in the induction of HO‐1 and p21. In summary, this study reveals that an increase in the level of HO‐1 markedly reduces the sensitivity of papillary thyroid carcinoma cells to apoptotic stimuli. The HO‐1 pathway of apoptosis resistance is associated with an increase in the levels of p21, involves a p38 MAPK and ERK‐mediated mechanism and can be suppressed by inhibiting NF‐kappaB. © 2004 Wiley‐Liss, Inc.
Application of ab initio theory to QSAR study of 1,4‐dihydropyridine‐based calcium channel blockers using GA‐MLR and PC‐GA‐ANN procedures
Authors: Hemmateenejad Bahram , Safarpour Mohammad A. , Miri Ramin , Taghavi Fariba 
Published: June 2004

AbstractThe usefulness of the quantum chemical descriptors, calculated at the level of the RHF theory using 6‐31G basis set for QSAR study of 1,4‐dihydropyridine‐based calcium channel antagonist was examined. A data set containing 45 dihydropyridine derivatives with known activity was used. Multiple linear regressions combined with genetic algorithm for variable selection and an artificial neural network model combined with principal component analysis for dimension reduction and genetic algorithm for factor selection (PC‐GA‐ANN) were employed. Some multiparametric MLR equations with good statistical quality were obtained for different classes of dihydropyridine derivatives. The resulting equations suggest that the electronic properties of the atoms belonging to the backbone of the molecules as well as the conformation of the molecules affect the binding of these molecules with their receptor. In the PC‐GA‐ANN, The principal components of the descriptors data matrix were used as the input of the neural network and then genetic algorithm was applied to select the most relevant set of principal components. Two ANN models with five selected principal components were obtained. These models, which have high statistical qualities, can predict the activity of the molecules with prediction errors lower than ±5%. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 1495–1503, 2004