bluuebunny/crossref_metadata_2025_split huggingface dataset:
Centrosome amplification induced by the antiretroviral nucleoside reverse transcriptase inhibitors lamivudine, stavudine, and didanosine
Authors: Yu Mia , Ward Yvona , Poirier Miriam C. , Olivero Ofelia A. 
Published: June 2009

AbstractIn cultured cells, exposure to the nucleoside reverse transcriptase inhibitor (NRTI) zidovudine (AZT) induces genomic instability, cell cycle arrest, micronuclei, sister chromatid exchanges, and shortened telomeres. In previous studies, we demonstrated AZT‐induced centrosome amplification (>2 centrosomes/cell). Here, we investigate centrosome amplification in cells exposed to other commonly used NRTIs. Experiments were performed using Chinese Hamster ovary (CHO) cells, and two normal human mammary epithelial cell (NHMEC) strains: M99005 and M98040, which are high and low incorporators of AZT into DNA, respectively. Cells were exposed for 24 hr to lamivudine (3TC), stavudine (d4T), didanosine (ddI), and thymidine, and stained with anti‐pericentrin antibody. Dose response curves were performed to determine cytotoxicity and a lower concentration at near plasma levels and a 10 fold higher concentration were chosen for the experiments. In CHO cells, there was a concentration‐dependent, significant (P< 0.05) increase in centrosome amplification for each of the NRTIs. In NHMEC strain M99005, an NRTI‐induced increase (P< 0.05) in centrosome amplification was observed for the high concentrations of each NRTI and the low doses of 3TC and ddI. In NHMEC strain M98040, the high doses of ddI and d4T showed significant increases in centrosome amplification. Functional viability of amplified centrosomes was assessed by arresting microtubule nucleation with nocodazole. In cells with more than two centrosomes, the ability to recover microtubule nucleation was similar to that of unexposed cells. We conclude that centrosome amplification is a consequence of exposure to NRTIs and that cells with centrosome amplification are able to accomplish cell division. Environ. Mol. Mutagen., 2009. © 2009 Wiley‐Liss, Inc.
Volatiles from leaves of field‐grown plants and shoot cultures of Gynura bicolor DC
Authors: Shimizu Yasuhiro , Imayoshi Yuriko , Kato Mika , Maeda Kazuhiro , Iwabuchi Hisakatsu , Shimomura Koichiro 
Published: June 2009

AbstractSystematic investigations of the volatiles of field‐grown plants and shoot cultures of Gynura bicolor have been conducted to obtain indispensable plant physiological information for propagating plants of consistent quality. Volatiles obtained by solvent‐assisted flavour evaporation (SAFE) of solvent extracts from leaves of commercial cultivars, shoot cultures and their regenerates were analysed using gas chromatography (GC), GC–mass spectrometry (GC–MS) and GC–olfactometry (GC–O). It was revealed for the first time that this plant had the following chemical characteristics: field‐grown plants, i.e. those plants commercially cultivated in three different regions of Japan and 7 month‐old regenerates of shoot cultures had almost the same GC profiles; their major components were (E)‐caryophyllene, α‐humulene and bicyclogermacrene; in contrast, the major components of the shoot cultures were (Z,E)‐α‐farnesene, (E)‐caryophyllene and α‐copaene. The biosynthetic pathways for the sesquiterpenes found in these materials were presumed from the analytical results. Aroma evaluations using GC–O revealed that 1‐octen‐3‐one, (Z)‐1,5‐octadien‐3‐one and trans‐4,5‐epoxy‐(E)‐2‐decenal were aroma‐impact compounds contributing to the characteristic metallic, green aroma, especially in the shoot cultures. In addition to these results, it was found that 2‐isopropyl‐ and 2‐isobutyl‐3‐methoxypyrazines were additional compounds related to the green, earthy aroma in the regenerates. These aroma‐impact compounds were detected only because of the GC–O analysis. Copyright © 2009 John Wiley & Sons, Ltd.
The detection of earnings manipulation: the three‐phase cutting plane algorithm using mathematical programming
Authors: Dikmen Burcu , Küçükkocaoğlu Güray 
Published: June 2009

AbstractThe primary goal of this study was to propose an algorithm using mathematical programming to detect earnings management practices. In order to evaluate the ability of this proposed algorithm, the traditional statistical models are used as a benchmark vis‐à‐vis their time series counterparts. As emerging techniques in the area of mathematical programming yield better results, application of suitable models is expected to result in highly performed forecasts. The motivation behind this paper is to develop an algorithm which will succeed in detecting companies that appeal to financial manipulation. The methodology is based on cutting plane formulation using mathematical programming. A sample of 126 Turkish manufacturing firms described over 10 financial ratios and indexes are used for detecting factors associated with false financial statements. The results indicate that the proposed three‐phase cutting plane algorithm outperforms the traditional statistical techniques which are widely used for false financial statement detections. Furthermore, the results indicate that the investigation of financial information can be helpful towards the identification of false financial statements and highlight the importance of financial ratios/indexes such as Days' Sales in Receivables Index (DSRI), Gross Margin Index (GMI), Working Capital Accruals to Total Assets (TATA) and Days to Inventory Index (DINV). Copyright © 2009 John Wiley & Sons, Ltd.
In vitro response of monocyte‐derived macrophages to a decellularized pericardial biomaterial
Authors: Ariganello Marianne B. , Labow Rosalind S. , Lee J. Michael 
Published: June 2009

AbstractDecellularized tissue‐derived heart valves are an example of biomaterials derived from natural scaffolds. These types of implants are increasing in popularity although their in vivo performance is still only poorly understood and has, at times, been catastrophic. It is apparent that better understanding is required before these biomaterials can be used safely. In this study, the human monocyte‐derived macrophage (MDM) response to decellularized bovine pericardium (DBP) was used as a model to predict the biological performance of these materials on implantation. Human monocytes differentiated on tissue culture polystyrene (TCPS) for 14 days were trypsinized and reseeded onto DBP, TCPS, and polydimethylsiloxane (PDMS) for 48 h. The MDMs on DBP contained less intracellular and extracellular esterase activity compared with MDMs on TCPS and PDMS, as well as less acid phosphatase activity than on TCPS. As well, morphologically, MDMs on DBP were less spread, less multinucleated and did not display many lamellipodia. Taken together, these data represent the first evidence of the MDM response to intact, native extracellular matrix, demonstrating that these cells reacted with an altered, possibly reduced foreign body response on this natural scaffold compared with the two control surfaces. This in vitro MDM cell model may provide a novel method for predicting and elucidating the biological performance of tissue‐derived biomaterials, thereby directing a more rational design of biomaterials for tissue regeneration purposes. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res 2010
Matrin 3: Chromosomal distribution and protein interactions
Authors: Zeitz Michael J. , Malyavantham Kishore S. , Seifert Brandon , Berezney Ronald 
Published: June 2009

AbstractMatrin 3 (matr3), an abundant protein of the internal nuclear matrix, has been linked to a variety of functional events. As a step toward defining its multifunctional nature, we have studied the association of matr3 with chromosome territories and identified potential interacting proteins. A similar staining pattern of matr3 was observed in fixed WI38 fibroblast cells and in live HeLa cells using a matr3‐GFP construct. Matr3 was detected throughout autosomal and the active X chromosome territories. Conversely, matr3 was strikingly excluded from the inactive X chromosome as well as within both the perinuclear and perinucleolar heterochromatin. Yeast two hybrid analysis identified matr3 interactions with 33 unique nuclear localized proteins and also revealed its propensity for self association. A majority of these proteins are involved in RNA metabolism and chromatin remodeling while others function in protein translation, DNA replication/repair and apoptosis. Further analysis of a selection of these proteins and scaffold attachment factor A (SAFA) by co‐localization and co‐immunoprecipitation experiments using HeLa cells confirmed their interactions with matr3. J. Cell. Biochem. 108: 125–133, 2009. © 2009 Wiley‐Liss, Inc.
On the road to understanding of the osteoblast adhesion: Cytoskeleton organization is rearranged by distinct signaling pathways
Authors: Zambuzzi Willian Fernando , Bruni‐Cardoso Alexandre , Granjeiro José Mauro , Peppelenbosch Maikel Petrus , de Carvalho Hernandes Faustino , Aoyama Hiroshi , Ferreira Carmen Veríssima 
Published: June 2009

AbstractPre‐osteoblast adhesion attracts increasing interest in both medicine and dentistry. However, how this physiological event alters osteoblast phenotype is poorly understood. We therefore attempted to address this question by investigating key biochemical mechanism that governs pre‐osteoblast adhesion on polystyrene surface. Importantly, we found that cofilin activity was strongly modulated by PP2A (Ser/Thr phosphatase), while cell‐cycle was arrested. Accordingly, we observed that the profile of cofilin phosphorylation (at Ser03) was similar to phospho‐PP2A (at Tyr307). Also, it is plausible to suggest during pre‐osteoblast adhesion that PP2A phosphorylation at Y307 was executed by phospho‐Src (Y416). In addition, it was observed that MAPKp38, but not MAPK‐erk, played a key role on pre‐osteoblast adhesion by phosphorylating MAPKAPK‐2 and ATF‐2 (also called CRE‐BP1). Also, the up‐modulation of RhoA reported here suggests its involvement at the beginning of osteoblast attachment, while Akt remained active during all periods. Altogether, our results clearly showed that osteoblast adhesion is under an intricate network of signaling molecules, which are responsible to guide their interaction with substrate mainly via cytoskeleton rearrangement. J. Cell. Biochem. 108: 134–144, 2009. © 2009 Wiley‐Liss, Inc.
NF‐kappa B is required for the development of tumor spheroids
Authors: Gallardo‐Pérez J.C. , Espinosa M. , Ceballos‐Cancino G. , Daniel A. , Rodríguez‐Enríquez S. , Aviles A. , Moreno‐Sánchez R. , Melendez‐Zajgla J. , Maldonado V. 
Published: June 2009

AbstractTumor cells cultured in three‐dimensional models provide a more realistic and biologically meaningful analysis of the initial phases of cancer development and drug resistance. Several studies have demonstrated that culture of cancer cells in three dimensions induces cellular resistance to a variety of anti‐neoplastic drugs by poorly understood mechanisms. The role of the transcription factor NF‐κB and inhibitors of apoptosis proteins (IAPs) in the onset and development of drug resistance during tumor spheroid growth has not been established. In this work, we found a significant increase in the activity and expression of NF‐κB and its downstream target XIAP (X‐linked IAP) in cancer cells grown as multi‐cellular tumor spheroids. Blocking XIAP expression with RNA interference markedly increased the sensitivity of cancer tumor spheroid cells toward anti‐neoplastic drugs, indicating a role for IAPs in establishing drug resistance. In turn, inhibition of NF‐κB by negative dominants suppressed spheroid formation, whereas overexpression of the upstream kinase IκBKβ increased their growth and resistance. The present data suggested that NF‐κB and its downstream target XIAP were essential for the growth and drug resistance of small avascular tumor. J. Cell. Biochem. 108: 169–180, 2009. © 2009 Wiley‐Liss, Inc.
PA‐MSHA inhibits proliferation and induces apoptosis through the up‐regulation and activation of caspases in the human breast cancer cell lines
Authors: Liu Zhe‐Bin , Hou Yi‐Feng , Min‐Dong  , Di Gen‐Hong , Wu Jiong , Shen Zhen‐Zhou , Shao Zhi‐Ming 
Published: June 2009

AbstractTo investigate the effects of PA‐MSHA (Pseudomonas aeruginosa‐mannose sensitive hemagglutinin) on inhibiting proliferation of breast cancer cell lines and to explore its mechanisms of action in human breast cancer cells. MCF‐10A, MCF‐7, MDA‐MB‐468, and MDA‐MB‐231HM cells were treated with PA‐MSHA or PA (Heat‐killed P. aeruginosa) at different concentrations and different times. Changes of cell super‐microstructure were observed by transmission electron microscopy. Cell cycle distribution and apoptosis induced by PA‐MSHA were measured by flow cytometry (FCM) with PI staining, ANNEXIN V‐FITC staining and Hoechst33258 staining under fluorescence microscopy. Western blot was used to evaluate the expression level of apoptosis‐related molecules. A time‐dependent and concentration‐dependent cytotoxic effect of PA‐MSHA was observed in MDA‐MB‐468 and MDA‐MB‐231HM cells but not in MCF‐10A or MCF‐7 cells. The advent of PA‐MSHA changed cell morphology, that is to say, increases in autophagosomes, and vacuoles in the cytoplasm could also be observed. FCM with PI staining, ANNEXIN V‐FITC and Hoechst33258 staining showed that the different concentrations of PA‐MSHA could all induce the apoptosis and G0–G1 cell cycle arrest of breast cancer cells. Cleaved caspase 3, 8, 9, and Fas protein expression levels were strongly associated with an increase in apoptosis of the breast cancer cells. There was a direct relationship with increased concentrations of PA‐MSHA but not of PA. Completely different from PA, PA‐MSHA may impart antiproliferative effects against breast cancer cells by inducing apoptosis mediated by at least a death receptor‐related cell apoptosis signal pathway, and affecting the cell cycle regulation machinery. J. Cell. Biochem. 108: 195–206, 2009. © 2009 Wiley‐Liss, Inc.
Polyamines affect histamine synthesis during early stages of IL‐3‐induced bone marrow cell differentiation
Authors: García‐Faroldi Gianni , Correa‐Fiz Florencia , Abrighach Hicham , Berdasco María , Fraga Mario F. , Esteller Manel , Urdiales José L. , Sánchez‐Jiménez Francisca , Fajardo Ignacio 
Published: June 2009

AbstractMast cells synthesize and store histamine, a key immunomodulatory mediator. Polyamines are essential for every living cell. Previously, we detected an antagonistic relationship between the metabolisms of these amines in established mast cell and basophilic cell lines. Here, we used the IL‐3‐driven mouse bone marrow‐derived mast cell (BMMC) culture system to further investigate this antagonism in a mast cell model of deeper physiological significance. Polyamines and histamine levels followed opposite profiles along the bone marrow cell cultures leading to BMMCs. α‐Difluoromethylornithine (DFMO)‐induced polyamine depletion resulted in an upregulation of histidine decarboxylase (HDC, the histamine‐synthesizing enzyme) expression and activity, accompanied by increased histamine levels, specifically during early stages of these cell cultures, where an active histamine synthesis process occurs. In contrast, DFMO did not induce any effect in either HDC activity or histamine levels of differentiated BMMCs or C57.1 mast cells, that exhibit a nearly inactive histamine synthesis rate. Sequence‐specific DNA methylation analysis revealed that the DFMO‐induced HDC mRNA upregulation observed in early bone marrow cell cultures is not attributable to a demethylation of the gene promoter caused by the pharmacological polyamine depletion. Taken together, the results support an inverse relationship between histamine and polyamine metabolisms during the bone marrow cell cultures leading to BMMCs and, moreover, suggest that the regulation of the histamine synthesis occurring during the early stages of these cultures depends on the concentrations of polyamines. J. Cell. Biochem. 108: 261–271, 2009. © 2009 Wiley‐Liss, Inc.
A new mechanism of gastric epithelial injury induced by acid exposure: The role of Egr‐1 and ERK signaling pathways
Authors: Abdel‐Latif Mohamed M.M. , Windle Henry J. , Davies Anthony , Volkov Yuri , Kelleher Dermot 
Published: June 2009

AbstractThe molecular mechanisms by which gastric acid causes epithelial injury in the stomach and initiates an inflammatory reaction are poorly understood. We aimed in the present study to investigate the role of the early growth response gene Egr‐1 and ERK in gastric epithelial cells following acid exposure, and the signaling pathways involved. Western blotting was used to assess Egr‐1 protein levels in AGS cells. A quantitative measurement of acid‐induced Egr‐1 and ERK translocation was performed using a high content analysis approach. Egr‐1 functionality was assessed by transient transfection with Egr‐1 antisense oligonucleotide. Exposure of AGS cells to acidic conditions induced Egr‐1 protein expression in a pH‐ and time‐dependent manner. Egr‐1 expression was markedly increased as the pH was reduced from pH 7.4 to 6.4. High content analysis of Egr‐1 activation showed acid‐induced Egr‐1 nuclear translocation; a maximum observed at 1–2 h followed by a decline to basal levels beyond 4 h. Acidic pH also activated ERK1/2 phosphorylation, whereas ERK1/2 inhibitors PD98059 and U0216 blocked both acid‐induced Egr‐1 and ERK translocation and expression. Moreover, acid exposure up‐regulated VEGF expression, which was inhibited by the Egr‐1 antisense oligonucleotide. Our results also demonstrate that exposure to acid induces Egr‐1 via MEK‐ERK1/2 pathway. These data suggest that Egr‐1 activation might play a crucial role in gastric mucosal inflammation and associated epithelial injury. J. Cell. Biochem. 108: 249–260, 2009. © 2009 Wiley‐Liss, Inc.
Thioredoxin interacting protein (TXNIP) induces inflammation through chromatin modification in retinal capillary endothelial cells under diabetic conditions
Authors: Perrone Lorena , Devi Takhellambam S. , Hosoya Ken‐ichi , Terasaki Tetsuya , Singh Lalit P. 
Published: June 2009

AbstractChronic hyperglycemia and activation of receptor for advanced glycation end products (RAGE) are known risk factors for microvascular disease development in diabetic retinopathy. Thioredoxin‐interacting protein (TXNIP), an endogenous inhibitor of antioxidant thioredoxin (TRX), plays a causative role in diabetes and its vascular complications. Herein we investigate whether HG and RAGE induce inflammation in rat retinal endothelial cells (EC) under diabetic conditions in culture through TXNIP activation and whether epigenetic mechanisms play a role in inflammatory gene expression. We show that RAGE activation by its ligand S100B or HG treatment of retinal EC induces the expression of TXNIP and inflammatory genes such as Cox2, VEGF‐A, and ICAM1. TXNIP silencing by siRNA impedes RAGE and HG effects while stable over‐expression of a cDNA for human TXNIP in EC elevates inflammation. p38 MAPK‐NF‐κB signaling pathway and histone H3 lysine (K) nine modifications are involved in TXNIP‐induced inflammation. Chromatin immunoprecipitation (ChIP) assays reveal that TXNIP over‐expression in EC abolishes H3K9 tri‐methylation, a marker for gene inactivation, and increases H3K9 acetylation, an indicator of gene induction, at proximal Cox2 promoter bearing the NF‐κB‐binding site. These findings have important implications toward understanding the molecular mechanisms of ocular inflammation and endothelial dysfunction in diabetic retinopathy. J. Cell. Physiol. 221: 262–272, 2009. © 2009 Wiley‐Liss, Inc
Hyperglycemia and mechanical stress: Targeting the renal podocyte
Authors: Lewko Barbara , Stepinski Jan 
Published: June 2009

AbstractHyperglycemia and deriving from glomerular hypertension mechanical stress are the key factors underlying pathogenesis of diabetic nephropathy (DN). Multiple direct and secondary effects of both these factors are mediated by complex signaling pathways with extensive interactions. The common signaling pathways stimulated by high glucose and mechanical insult may act in an additive manner, thereby accelerating the cell damage. Podocytes, the cells covering the outer aspect of glomerular basement membrane (GBM), are subjected not only to the load of filtered glucose but also to diverse mechanical forces. Bulging into the Bowman's space, they have no support from the apical side, which makes them particularly susceptible to the effects of mechanical strain. Both high glucose and mechanical stress may impair the protein systems anchoring the podocyte foot processes in GBM, therefore blunting resistance of these cells to mechanical forces. Modulation by these factors of expression and activity of numerous structural and functional proteins results in the (auto)inflammatory responses, dysfunction, apoptosis or necrosis of the podocytes. Loss of the podocytes is irreversible due to their inability to proliferate and to replenish damaged cells. Podocytes are injured early in the course of DN, which, most likely, underlies further glomerular and renal damage in diabetes. This review summarizes the effects of elevated glucose and mechanical stress that seem to be involved in podocyte impairment in diabetes, with particular focus on the possible interactions between these factors. J. Cell. Physiol. 221: 288–295, 2009. © 2009 Wiley‐Liss, Inc.
Non‐selective cation channel activity is required for lysophosphatidylcholine‐induced monocyte migration
Authors: Schilling Tom , Eder Claudia 
Published: June 2009

AbstractLysophosphatidylcholine (LPC) is a major atherogenic lipid which stimulates the recruitment of monocytes to atherosclerotic lesions. The physiological mechanisms underlying LPC‐induced monocyte migration are poorly understood. Here we demonstrate that LPC activates non‐selective cation channels, which are significantly involved in LPC‐induced chemotaxis of monocytes. External LPC elicited the activation of non‐selective cation currents in THP‐1 monocytes, which occurred in a G protein and phospholipase C‐independent manner. LPC‐activated currents were almost completely inhibited by Gd3+, La3+, and TRAM‐34. Furthermore, currents were partially reduced by either 2‐aminoethoxydiphenyl borate (2‐APB) or ruthenium red, while combined application of 2‐APB and ruthenium red abolished LPC‐activated currents. The 2‐APB‐sensitive current component was potentiated by flufenamic acid and Ca2+‐free extracellular solution, while the ruthenium red‐sensitive current component was abolished by capsazepine. This pharmacological profile suggests that LPC simultaneously activates TRPC6 and TRPV1 channels in monocytes. Furthermore, in the presence of Gd3+, La3+, TRAM‐34, 2‐APB, ruthenium red or capsazepine, LPC‐induced chemotaxis of monocytes was substantially inhibited, indicating that activation of both channel types is required for optimal migration of LPC‐stimulated monocytes. Thus, ion channel inhibition may represent a powerful strategy to attenuate the progression of atherosclerosis by reducing monocyte infiltration. J. Cell. Physiol. 221: 325–334, 2009. © 2009 Wiley‐Liss, Inc.