bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amine‐Functionalised Hexagonal Mesoporous Silica as Support for Copper(II) Acetylacetonate Catalyst
Authors: Silva Ana Rosa , Wilson Karen , Whitwood Adrian C. , Clark James H. , Freire Cristina 
Published: January 2006

AbstractCopper(II) acetylacetonate was anchored onto a hexagonal mesoporous silica (HMS) material using a two‐step procedure: (i) functionalisation of the surface hydroxy groups with (3‐aminopropyl)triethoxysilane (AMPTSi) and then (ii) anchoring of the copper(II) complex through Schiff condensation with free amine groups, using two different metal complex loadings. Upon the first step, nitrogen elemental analysis, XPS and DRIFT showed the presence of amine groups on the surface of the HMS material, and porosimetry indicated that the structure of the mesoporous material remained unchanged, although a slight decrease in surface area was observed. Atomic absorption, XPS and DRIFT showed that copper(II) acetylacetonate was anchored onto the amine‐functionalised HMS by Schiff condensation between the free amine groups and the carbonyl groups of the copper(II) complex; using EPR an NO3 coordination sphere was proposed for the anchored copper(II) complex. The new [Cu(acac)2]AMPTSi/HMS materials were tested in the aziridination of styrene at room temperature, using PhI=NTs as nitrogen source and acetonitrile as solvent. The styrene conversion and total TON of the heterogeneous phase reaction are higher than those of the same reaction catalysed in homogeneous phase by [Cu(acac)2]; nevertheless, the initial activity decreases and the reaction time increases due to substrate and product diffusion limitations. The heterogeneous catalyst showed a successive slight decrease in catalytic activity when reused for two more times.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Methyl‐Hydroxypyridinecarboxylic Acids as Possible Bidentate Chelating Agents for Aluminium(III): Synthesis and Metal–Ligand Solution Chemistry
Authors: Di Marco Valerio B. , Dean Annalisa , Ferlin Maria Grazia , Yokel Robert A. , Li Haitao , Venzo Alfonso , Bombi G. Giorgio 
Published: January 2006

AbstractIn view of a possible application to aluminium chelation therapy, 1‐methyl‐3‐hydroxy‐4‐pyridinecarboxylic acid (1M3H4P) and 1‐methyl‐4‐hydroxy‐3‐pyridinecarboxylic acid (1M4H3P) were synthesized, and their chemical interactions with aluminium(III) were investigated in aqueous 0.6 m (Na)Cl at 25 °C by means of potentiometric titrations. The qualitative and quantitative results obtained were confirmed by UV spectrophotometry and 1H NMR spectroscopy. For both ligands, the species AlL2+, AlL2+, AlL3, and AlL2H–1 were identified, with logβ1,1,0 = 7.66, logβ1,2,0 = 14.27, logβ1,3,0 = 19.099, and logβ1,2,–1 = 7.00 for 1M3H4P, logβ1,1,0 = 7.21, logβ1,2,0 = 13.41, logβ1,3,0 = 18.15, and logβ1,2,–1 = 6.4 for 1M4H3P. The chelation strength of 1M3H4P and 1M4H3P is lower than that of other available aluminium(III) chelators, e.g. deferiprone (pAl difference at physiological pH: ca. 3 log units). The octanol/aqueous partitioning values of 1M3H4P and 1M4H3P were 0.0054 and 0.0015, respectively, showing high hydrophilicity. The efficiencies of the ligands to chelate aluminium(III) were evaluated at physiological pH and ion strength “in vitro”. 1M3H4P and 1M4H3P were more effective than their non‐methylated analogs 3H4P and 4H3P. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
A Mild Chemo‐Enzymatic Oxidation–Hydrocyanation Protocol
Authors: Vugts Danielle J. , Veum Lars , al‐Mafraji Kanar , Lemmens Renske , Schmitz Rob F. , de Kanter Frans J. J. , Groen Marinus B. , Hanefeld Ulf , Orru Romano V. A. 
Published: January 2006

AbstractOxidation–hydrocyanation of γ,δ‐unsaturated alcohols using (immobilised) TEMPO/PhI(OAc)2 in combination with HbHNL proceeds smoothly. After (in situ) protection, the resulting cyanohydrin derivatives were obtained in good overall yields and high ee’s. A mild TEMPO‐catalysed oxidation protocol is described that yields β,γ‐unsaturated aldehydes without isomerisation of the double bond and that is compatible with a subsequent HbHNL‐catalysed hydrocyanation performed in the same solvent system. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Calcyclin binding protein promotes DNA synthesis and differentiation in rat neonatal cardiomyocytes
Authors: Au Ka‐Wing , Kou Cecy Y.C. , Woo Anthony Y.H. , Chim Stephen S.C. , Fung Kwok‐Pui , Cheng Christopher H.K. , Waye Mary M.Y. , Tsui Stephen K.W. 
Published: January 2006

AbstractDuring cardiac muscle development, most cardiomyocytes permanently withdraw from the cell cycle. Previously, by suppressive subtractive hybridization, we identified calcyclin‐binding protein/Siah‐interacting protein (CacyBP/SIP) as one of the candidates being upregulated in the hyperplastic to hypertrophic switch, suggesting an important role of CacyBP/SIP in cardiac development. To show the importance of CacyBP/SIP during myoblast differentiation, we report here that CacyBP/SIP is developmentally regulated in postnatal rat hearts. The overexpression of CacyBP/SIP promotes the differentiation and DNA synthesis of H9C2 cells and primary rat cardiomyocytes, as well as downregulates the expression of β‐catenin. Besides, CacyBP/SIP promotes the formation of myotubes and multinucleation upon differentiation. To investigate the cardioprotective role of CacyBP/SIP in cardiomyocytes, a hypoxia/reoxygenation model was employed. We found that CacyBP/SIP was upregulated during myocardial infarction (MI) and hypoxia/reoxygenation. As a conclusion, CacyBP/SIP may play a role in cardiomyogenic differentiation and possibly protection of cardiomyocytes during hypoxia/reoxygenation injury. J. Cell. Biochem. 98: 555–566, 2006. © 2006 Wiley‐Liss, Inc.
Activin A induces erythroid gene expressions and inhibits mitogenic cytokine‐mediated K562 colony formation by activating p38 MAPK
Authors: Huang Huei‐Mei , Chiou Huei‐Yu , Chang Ju‐Ling 
Published: January 2006

AbstractActivin A, a member of the transforming growth factor (TGF)‐β superfamily, is involved in the regulation of erythroid differentiation. Previous studies have shown that activin A inhibited the colony‐forming activity of mouse Friend erythroleukemia cells, however, the mechanism remains unknown. First, we show herein that activin A induced the expression and activated the promoters of α‐globin and ζ‐globin in K562 cells, confirming that activin A induces erythroid differentiation in K562 cells. The p38 mitogen activated protein kinase (MAPK) inhibitor, SB203580, inhibited and the extracellular signal regulated kinase (ERK) inhibitor, PD98059, enhanced the expression and promoter activities of α‐globin and ζ‐globin by activin A, indicating that p38 MAPK and ERK are crucial for activin A‐induced erythroid genes expression. Second, SB203580 inhibited the inhibitory effect of activin A on the colony‐forming activity of K562 cells using the methylcellulose colony assay, indicating that activin A inhibits K562 colony formation by activating p38 MAPK. In addition, mitogenic cytokines SCF, IL‐3, and GM‐CSF induced colony formation of K562 cells that could be inhibited by PD98059 or enhanced by SB203580, respectively, indicating that these mitogenic cytokines induce K562 colony formation by activating ERK and inactivating p38 MAPK. Furthermore, activin A reduced the induction effect of these mitogenic cytokines on K562 colony formation in a dose‐dependent manner. The inhibition of p38 MAPK reverted the inhibitory effect of activin A on mitogenic cytokine‐mediated K562 colony formation. We conclude that activin A can regulate the same pathway via p38 MAPK to coordinate cell proliferation and differentiation of K562 cells. J. Cell. Biochem. 98: 789–797, 2006. © 2006 Wiley‐Liss, Inc.
DNA vaccines: Successes and limitations in cancer and infectious disease
Authors: Lowe Devin B. , Shearer Michael H. , Kennedy Ronald C. 
Published: January 2006

AbstractVaccination with plasmid DNA is an active area of investigation that is being applied to diseases including cancer and microbial pathogens associated with infectious diseases. Since its discovery, great progress has been made with the administration of DNA vaccines to initiate specific and effective immune responses against targeted illnesses. However, many obstacles still face its use in prophylactic and therapeutic vaccination scenarios. The nature of these difficulties alongside the successes and future of plasmid DNA will be discussed. J. Cell. Biochem. 98: 235–242, 2006. © 2006 Wiley‐Liss, Inc.
Defining the transcriptome of accelerated and replicatively senescent keratinocytes reveals links to differentiation, interferon signaling, and Notch related pathways
Authors: Perera Ranjan J. , Koo Seongjoon , Bennett C. Frank , Dean Nicholas M. , Gupta Nitin , Qin Jian‐Zhong , Nickoloff Brian J. 
Published: January 2006

AbstractEpidermal keratinocytes (KCs) undergo highly orchestrated morphological and molecular changes during transition from proliferative compartment into growth arrested early and late differentiation layers, prior to dying in outermost cornified layers of normal skin. Creation of stratum corneum is vital to barrier function protecting against infection. Transcriptional events in KCs regulating complex processes of differentiation and host defense required to maintain constant epidermal thickness and resistance to infection in either young or aged skin are largely unknown. Furthermore, as terminal differentiation is characterized by irreversible loss of replicative potential culminating in dead layers at the skin surface, this process may be viewed as a form of senescence. However, a complete transcriptional profile of senescent (SN) human KCs has not been previously defined to permit delineation of molecular boundaries involving differentiation and senescence. To fill this void, we utilized global transcriptional analysis of KCs maintained in vitro as either cultures of proliferating (PR) cells, early and late confluent (LC) (accelerated senescence) cultures, or KCs undergoing replicative senescence. Global gene expression profiling revealed early confluent (EC) KCs were somewhat similar to PR KCs, while prominent differences were evident when compared to LC KCs; which were also distinct from replicatively SN KCs. While confluent KCs have in common several genes regulating differentiation with replicatively SN KCs, the latter cells expressed elevated levels of genes involved in interferon signaling and inflammatory pathways. These results provide new insights into cell autonomous transcriptional‐based programs operative within KCs contributing to replicative senescence, with partial sharing of genes involved in differentiation. In addition, regulation of KC senescence may involve participation of interferon signaling pathways derived from the important role of KCs in protecting skin from infection. Integrating all of the transcriptional data revealed a key role for Notch receptor mediated signaling in the confluency induced differentiation phenotype using this model system. J. Cell. Biochem. 98: 394–408, 2006. © 2006 Wiley‐Liss, Inc.
c‐Jun kinase mediates expression of VEGF induced at transcriptional level by Rac1 and Cdc42Hs but not by RhoA
Authors: Saníger M. Luisa , Oya Ricardo , Macías David , Domínguez Jorge N. , Aránega Amelia , Luque Francisco 
Published: January 2006

AbstractTumour angiogenesis is mediated by increased levels of vascular endothelial growth factor (VEGF). We have studied the mechanism by which endogenous activation of Rho oncoproteins regulates VEGF expression in COS‐7 and NIH3T3 cells. We carried out transient and stable transfection with constitutively activated rhoA, rac1, and cdc42 mutants in COS‐7 and NIH3T3 cells, respectively in the absence of external stimuli. Western blot and inmunohistochemistry assays of those cells revealed increased VEGF protein expression. Cotransfection with constitutively activated rhoA, rac1, and cdc42 mutants and a VEGF promoter‐reporter construct showed an increase in VEGF promoter transcriptional activity induced by Rho oncoproteins in COS‐7 and NIH3T3. c‐Jun kinase had been described as a MAPK involved in Rho oncoproteins pathways. Interestingly, we found that c‐Jun kinase chemical inhibition as well as transient transactivation assays using dominant negative c‐Jun kinase mutant abolished the VEGF promoter transcriptional induction by Rac1 and Cdc42 but not by RhoA. These findings indicate that Rho oncoprotein endogenously activated regulates VEGF expression through a transcriptional mechanism, and that the c‐Jun kinase activity is a mediator in the expression of VEGF induced by Rac1 and Cdc42 oncoproteins, but not of that induced by RhoA. J. Cell. Biochem. 98: 650–660, 2006. © 2006 Wiley‐Liss, Inc.
DNA sequences acting as binding sites for NM23/NDPK proteins in melanoma M14 cells
Authors: Cervoni Laura , Egistelli Lorenza , Eufemi Margherita , d'Abusco Anna Scotto , Altieri Fabio , Lascu Ioan , Turano Carlo , Giartosio Anna 
Published: January 2006

AbstractWe isolated and analyzed by chromatin immunoprecipitation (ChIP) in viable M14 cells DNA sequences bound to the antimetastatic protein nucleoside diphosphate kinase (NM23/NDPK) to shed some light on the nuclear functions of this protein and on the mechanism by which it acts in development and cancer. We assessed the presence of selected sequences from promoters of platelet‐derived growth factor A (PDGF‐A), c‐myc, myeloperoxidase (MPO), CD11b, p53, WT1, CCR5, ING1, and NM23‐H1 genes in the cross‐linked complexes. Quantitative PCR (Q‐PCR) showed a substantial enrichment of the correlated oncosuppressor genes p53, WT1, ING1, and NM23‐H1 in the immunoprecipitated (IP) DNA. This suggests that NM23/NDPK binding is involved in the transcription regulation of these genes. These results reveal new interactions that should help us to disclose the antimetastatic mechanism of NM23. J. Cell. Biochem. 98: 421–428, 2006. © 2006 Wiley‐Liss, Inc.
RNAi‐mediated silencing of insulin receptor substrate 1 (IRS‐1) enhances tamoxifen‐induced cell death in MCF‐7 breast cancer cells
Authors: Cesarone Gregory , Garofalo Cecilia , Abrams Marc T. , Igoucheva Olga , Alexeev Vitali , Yoon Kyonggeun , Surmacz Eva , Wickstrom Eric 
Published: January 2006

AbstractInsulin receptor substrate 1 (IRS‐1) is a major downstream signaling protein for insulin and insulin‐like growth factor I (IGF‐I) receptors, conveying signals to PI‐3K/Akt and ERK1/2 pathways. In breast cancer, IRS‐1 overexpression has been associated with tumor development, hormone‐independence and antiestrogen‐resistance. In part, these effects are related to potentiation of IRS‐1/PI‐3K/Akt signaling. In estrogen sensitive breast cancer cell lines, tamoxifen treatment reduces IRS‐1 expression and function; consequently, inhibiting IRS‐1/PI‐3K signaling. We tested whether anti‐IRS1 siRNA could inhibit growth and survival of estrogen‐sensitive MCF‐7 breast cancer cells, when used alone or in combination with TAM. Our results indicated: (a) out of four tested anti‐IRS1 siRNAs, two siRNAs reduced IRS‐1 protein by approximately three‐fold in both growing and IGF‐I‐stimulated cells without affecting a closely related protein, IRS‐2; (b) these effects paralleled IRS1 mRNA downregulation by approximately three‐fold, measured by quantitative real time‐polymerase chain reaction; (c) action of anti‐IRS1 siRNAs induced the apoptotic response, observed by altered mitochondrial membrane potential coupled with downregulation of NF‐κB target Bcl‐xL and reduced cell viability; (d) anti‐IRS1 siRNA treatment enhanced the cytotoxic effects of TAM by ∼20%. In summary, anti‐IRS1 RNAi strategy could become a potent tool to induce breast cancer cell death, especially if combined with standard TAM therapy. J. Cell. Biochem. 98: 440–450, 2006. © 2006 Wiley‐Liss, Inc.
PECAM‐1 isoform‐specific activation of MAPK/ERKs and small GTPases: Implications in inflammation and angiogenesis
Authors: Wang Yongji , Sheibani Nader 
Published: January 2006

AbstractPlatelet‐endothelial cell adhesion molecule‐1 (PECAM‐1/CD31) is expressed on the surface of endothelial cells (EC) and leukocytes. PECAM‐1 plays an important role in endothelial‐leukocyte and endothelial‐endothelial cell–cell interactions. The anti‐PECAM‐1 antibody‐mediated blockade of these interactions inhibits transendothelial migration (TEM) of leukocytes and angiogenesis. PECAM‐1 may accommodate these processes through the regulation of cell adhesive and migratory mechanisms. How PECAM‐1 regulates these dynamic processes remain unknown. Here we show that PECAM‐1 transduces outside‐in signals, which activate MAPK/ERKs and small GTPases. This occurs through PECAM‐1‐mediated formation of intracellular‐signaling complexes, Shc/Grb2/SOS1 and/or Crkl/C3G, which is initiated by PECAM‐1 engagement on the surface of leukocytes and/or EC. Src, SHP2, and alternative PECAM‐1 pre‐mRNA splicing play a regulatory role in these signaling events. Our findings reveal that PECAM‐1 engagement on the cell surface can transduce “outside‐in” signals and activate MAPK/ERKs and small GTPases, impacting both cadherin‐mediated cell–cell and integrin‐mediated cell–matrix interactions. Thus, we propose PECAM‐1 is an important mediator of vascular barrier and regulator of leukocyte and EC adhesion and migration. J. Cell. Biochem. 98: 451–468, 2006. © 2006 Wiley‐Liss, Inc.
A gene expression signature that distinguishes desmoid tumours from nodular fasciitis
Authors: Bacac M , Migliavacca E , Stehle J‐C , McKee T , Delorenzi M , Coindre J‐M , Guillou L , Stamenkovic I 
Published: January 2006

AbstractNodular fasciitis (NF) is a rapidly growing cellular mass composed of fibroblasts/myofibroblasts, usually localized in subcutaneous tissues, that typically undergoes fibrosis and almost never recurs. Desmoid tumours (DTs) are rare forms of fibroblastic/myofibroblastic growth that arise in deep soft tissues, display a propensity for local infiltration and recurrence, but fail to metastasize. Given that both entities are primarily fibroblastic/myofibroblastic lesions with overlapping histological features, their gene expression profiles were compared to identify differentially expressed genes that may provide not only potential diagnostic markers, but also clues as to the pathogenesis of each disorder. Differentially expressed transcripts (89 clones displaying increased expression in DTs and 246 clones displaying increased expression in NF) included genes encoding several receptor and non‐receptor tyrosine kinases (EPHB3, PTPRF, GNAZ, SYK, LYN, EPHA4, BIRC3), transcription factors (TWIST1, PITX2, EYA2, OAS1, MITF, TCF20), and members of the Wnt signalling pathway (AXIN2, WISP1, SFRP). Remarkably, almost one‐quarter of the differentially expressed genes encode proteins associated with inflammation and tissue remodelling, including members of the interferon (IFN), tumour necrosis factor (TNF), and transforming growth factor beta (TGF‐β) signalling pathways as well as metalloproteinases (MMP1, 9, 13, 23), urokinase plasminogen activator (PLAU), and cathepsins. The observations provide the first comparative molecular characterization of desmoid tumours and nodular fasciitis and suggest that selected tyrosine kinases, transcription factors, and members of the Wnt, TGF‐β, IFN, and TNF signalling pathways may be implicated in influencing and distinguishing their fate. Copyright © 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Active center determinations on MgCl2‐supported fourth‐ and fifth‐generation Ziegler–Natta catalysts for propylene polymerization
Authors: Yaluma Andrew K. , Tait Peter J. T. , Chadwick John C. 
Published: January 2006

AbstractActive center determinations on different Ziegler–Natta polypropylene catalysts, comprising MgCl2, TiCl4, and either a diether or a phthalate ester as internal donor, have been carried out by quenching propylene polymerization with tritiated ethanol, followed by radiochemical analysis of the resulting polymers. The purpose of this study was to determine the factors contributing to the high activities of the catalyst system MgCl2/TiCl4/diether—AlEt3. Active center contents (C*) in the range 2–8% (of total Ti present) were measured and a strong correlation between catalyst activity and active center content was found, indicating that the high activity of the diether‐containing catalysts is due to an increased proportion of active centers rather than to a difference in propagation rate coefficients. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 1635–1647, 2006
Polypyrrole/poly(N‐isopropylacrylamide‐co‐acrylic acid) thermosensitive and electrically conductive composite microgels
Authors: Lin Chia‐Lung , Chiu Wen‐Yen 
Published: January 2006

AbstractThe electrically conductive polypyrrole/dodecylbenzene sulfonic acid/poly(N‐isopropylacrylamide‐co‐acrylic acid) (PPy/DBSA/poly(NIPAAm‐co‐AA)) composite microgels were synthesized by a chemical oxidation of pyrrole in the presence of DBSA as the primary dopant, and poly(NIPAAm‐co‐AA) microgels as the polymeric codopant and template, in which APS was used as the oxidant. It was proposed to prepare “intelligent” polymer microgel particles containing both thermosensitive and electrically conducting properties. The polymerization of pyrrole took place directly inside the microgel networks, leading to formation of composite microgels and the morphology was observed by transmission electron microscope. PPy particles interacted strongly with microgels, as the acid groups of microgels acted as the polymeric codopant. The composite microgels thus formed showed electrically conducting behavior dependent on humidity and temperature. At temperatures lower than lower critical solution temperature, the conductivity decreased with increasing the humidity and a small hysteresis phenomenon was observed. The hysteresis became indistinct when temperature was near volume phase transition temperature. However, after the treatment of high temperature and high humidity, the conductivity increased surprisingly due to the structure reorganization inside the composite microgels. The distinctive functionality of the PPy composite microgels was expected to be utilized in many attractive applications. © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 1648–1659, 2006
Synthesis of A2B star block copolymers from a heterotrifunctional initiator
Authors: Glaied O. , Delaite C. , Dumas P. 
Published: January 2006

AbstractWe described the obtention of A2B star block copolymers through the use of a new heterotrifunctional initiator. That way, well‐defined (PCL)2‐arm‐PtBuMA and (PCL)2‐arm‐PS star block copolymers have been synthesized from a heterotrifunctional initiator bearing two hydroxyl groups able to initiate ROP of CL (with AlEt3 or Sn(Oct)2 as coinitiator) and a bromide function able to initiate ATRP of tBuMA or styrene. Firstly, we have proceeded using a sequential process (two‐steps), leading to an intermediate macroinitiator. Secondly, attempt to polymerize these two monomers in a simultaneous process (one‐step), that is directly from the mixture of monomers, initiator, coinitiators, and solvent, has been realized and has shown that some interferences between the two polymerizations occurred, leading to an inhibition of ATRP when Sn(Oct)2 was used and an unexpected increase in control when AlEt3 was used as catalyst for the ROP (obtention of well‐defined (PCL)2‐arm‐PtBuMA with pdi of 1.18). © 2006 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 44: 1796–1806, 2006