bluuebunny/crossref_metadata_2025 huggingface dataset:
Preformed microspherical inclusions for rheological control and physical property modification of epoxy resins
Authors: Frigione M. , Calò E. , Maffezzoli A. , Acierno D. , Carfagna C. , Ambrogi V.
Published: January 2006

Epoxy microspheres, with average diameters in the order of 4–5 μm, were first produced as insoluble gel resulting from the reactions of a bisphenolic epoxy resin with an aromatic hardener in solution. They were then used as reactive flow modifiers and toughening agents for bisphenolic epoxy resins with same chemical composition. Thermal analysis, rheological measurements, and impact tests were performed to assess their ability to modify the viscosity of the uncured resin and to determine the effects on the cured resins with respect to the glass transition temperature and impact strength. Two similar epoxy systems modified with the addition of different amounts of microspheres preserve the glass transition temperature of the cured unmodified epoxy. The addition of microspheres is responsible for secondary transition. The addition of a small fraction of microspheres does not affect the reactivity of the epoxy resin, while the inclusion of a higher content leads to a noticeable reduction in the gel time of the epoxy systems, indicating that microspheres are not inert fillers. Finally, a limited enhancement of the toughness of the epoxy resin was observed, as a consequence of strong interactions between the matrix and the microspheres. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 100: 748–757, 2006
Preparation of polysulfone hollow fiber affinity membrane modified with mercapto and its recovery properties. I. Synthesis and preparation of hollow fiber matrix membrane
Authors: Wang Bing , Cheng Bowen , Cui Yongfang
Published: January 2006

Several kinds of chloromethyl polysulfones (CMPSF) with different chlorinity and reactive groups were synthesized by Friedel‐Crafts reaction, which could be utilized as reactively matrix membrane materials. The CMPSF hollow matrix membranes were prepared with phase inversion by utilization of the CMPSF/additive/DMAC casting solution and CMPSF as membrane materials. The rheological behavior of CMPSF/additives/DMAC spinning casting solution was studied. The experimental results showed that the spinning casting solution was a pseudoplastic fluid, the apparent viscosity of the spinning casting solution decreased with the increase of shearing rate, and the viscous flow activity energy of the spinning casting solution was inclined to unchange at high shearing rate. The effects of composition of spinning casting solution and process parameters of dry–wet spinning on the structure of CMPSF hollow fiber matrix membrane were investigated. The pore size, porosity, and water flux of membrane decreased with the increase of additive content, bore liquid, and dry spinning distance. With the increase of extrusion volume outflow, the external diameter, wall thickness, and porosity of the hollow fiber matrix membrane increased, but the pore size and water flux of the membrane decreased. It was also found that the effects of internal coagulant composition and external coagulant composition on the structure of CMPSF hollow fiber matrix membrane were different. The experimental results showed that thermal drawing could increase the mechanical properties of CMPSF hollow fiber matrix membrane and decrease the pore size, porosity, and water flux of the CMPSF hollow fiber matrix membrane, and the thermal treatment could increase the homogeneity and stability of the structure of the CMPSF hollow fiber matrix membrane. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 100: 758–771, 2006
Synthesis of polyethylene oxide end‐capped with perfluoroalkyl groups/polystyrene prototype brushes
Authors: Ishizu Koji , Yamada Hiroe , Toyoda Keiichi , Furukawa Taiichi
Published: January 2006

Polystyrene (PS)/poly(ethylene oxide) (PEO) prototype brushes were prepared by alternating free‐radical copolymerization of methacryloyl‐terminated PS and α‐vinylbenzyl‐ω‐hydroxy or α‐vinylbenzyl‐ω‐perfluoroalkyl (Rf) PEO macromonomers with the addition of Lewis acid (SnCl4). It was found from their dilute‐solution properties that PS/PEO end‐capped with Rf (PBRf), and PS/PEO having OH groups at terminal ends (PBOH) prototype brushes formed a single molecule in benzene and aggregates in chloroform, respectively. However, the brush PBOH formed a single molecule in N,N‐dimethylformamide. Such aggregation behaviors seemed to be caused by the interaction between hydroxy groups of PEO chain ends. The brush PBOH was also converted into PBRf‐type brush by chemical modification, using corresponding acid chloride. The substitution of Rf groups was ∼70% due to slipping of terminal hydroxy groups into PEO internal domains. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 100: 772–778, 2006
Recovery of scrap iron metal value using biogenerated ferric iron
Authors: Ballor Nicholas R. , Nesbitt Carl C. , Lueking Donald R.
Published: January 2006

The utility of employing biogenerated ferric iron as an oxidant for the recycling of scrap metal has been demonstrated using continuously growing cells of the extremophilic organism Acidithiobacillus ferrooxidans. A ferric iron rich (70 mol%) lixiviant resulting from bioreactor based growth of A. ferrooxidans readily solubilized target scrap metal with the resultant generation of a leachate containing elevated ferrous iron levels and solubilized copper previously resident in the scrap metal. Recovery of the copper value was easily accomplished via a cementation reaction and the clarified leachate containing a replenished level of ferrous iron as growth substrate was shown to support the growth of A. ferrooxidans and be fully recyclable. The described process for scrap metal recycling and copper recovery was shown to be efficient and economically attractive. Additionally, the utility of employing the Eh of the growth medium as a means for monitoring fluctuations in cell density in cultures of A. ferrooxidans is demonstrated. © 2006 Wiley Periodicals, Inc.
Projections of the sensory trigeminal nucleus in a percomorph teleost, tilapia (Oreochromis niloticus)
Authors: Xue Hao‐Gang , Yamamoto Naoyuki , Yang Chun‐Ying , Kerem Gulnisa , Yoshimoto Masami , Sawai Nobuhiko , Ito Hironobu , Ozawa Hitoshi
Published: January 2006

The sensory trigeminal nucleus of teleosts is the rostralmost nucleus among the trigeminal sensory nuclear group in the rhombencephalon. The sensory trigeminal nucleus is known to receive the somatosensory afferents of the ophthalmic, maxillar, and mandibular nerves. However, the central connections of the sensory trigeminal nucleus remain unclear. Efferents of the sensory trigeminal nucleus were examined by means of tract‐tracing methods, in a percomorph teleost, tilapia. After tracer injections to the sensory trigeminal nucleus, labeled terminals were seen bilaterally in the ventromedial thalamic nucleus, periventricular pretectal nucleus, medial part of preglomerular nucleus, stratum album centrale of the optic tectum, ventrolateral nucleus of the semicircular torus, lateral valvular nucleus, prethalamic nucleus, tegmentoterminal nucleus, and superior and inferior reticular formation, with preference for the contralateral side. Labeled terminals were also found bilaterally in the oculomotor nucleus, trochlear nucleus, trigeminal motor nucleus, facial motor nucleus, facial lobe, descending trigeminal nucleus, medial funicular nucleus, and contralateral sensory trigeminal nucleus and inferior olive. Labeled terminals in the oculomotor nucleus and trochlear nucleus showed similar densities on both sides of the brain. However, labelings in the trigeminal motor nucleus, facial motor nucleus, facial lobe, descending trigeminal nucleus, and medial funicular nucleus showed a clear ipsilateral dominance. Reciprocal tracer injection experiments to the ventromedial thalamic nucleus, optic tectum, and semicircular torus resulted in labeled cell bodies in the sensory trigeminal nucleus, with a few also in the descending trigeminal nucleus. J. Comp. Neurol. 495:279–298, 2006. © 2006 Wiley‐Liss, Inc.
Programmed Helicity in Self‐Assembled Hydrogen‐Bonded Chains of Chiral Copper(II) Complexes
Authors: Lonnon David G. , Colbran Stephen B. , Craig Donald C.
Published: January 2006

The copper(II) complexes [Cu(H2L1)Cl2]2[CuCl4]·CH3CN·H2O (HL1 = N‐6‐(4‐hydroxyphenyl)‐2‐pyridylmethyl‐N,N′,N′‐trimethylethylenediamine), [Cu(HL2)Cl2] (HL2 = N‐4‐hydroxybenzylmethyl‐N,N′,N′‐trimethylethylenediamine)and [Cu2(μ‐L3)2(H2O)(ClO4)]ClO4·H2O (HL3 = N‐2‐hydroxybenzylmethyl‐N,N′,N′‐trimethylethylenediamine) were prepared and characterised in acetonitrile solution (by ESI‐MS, EPR and UV/Vis‐NIR spectroscopy) and in the solid state (by X‐ray crystallography). Each copper(II) complex is chiral and has a potential inter‐complex hydrogen‐bond donor group. Upon crystallisation, all three copper(II) complexes undergo spontaneous enantioselective self‐assembly into hydrogen‐bond‐linked helices.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Metal‐Free Catalytic Nucleophilic Substitution of Propargylic Alcohols
Authors: Sanz Roberto , Martínez Alberto , Álvarez‐Gutiérrez Julia M. , Rodríguez Félix
Published: January 2006

Organic acids such as PTS efficiently catalyze direct nucleophilic substitutions of the hydroxy groups of propargylic alcohols with a large variety of carbon‐ and heteroatom‐centered nucleophiles. Reactions can be conducted under mild conditions and in air without the need for dried solvents. Reactions on multigram scales are also possible. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Quantifying effects of ligands on androgen receptor nuclear translocation, intranuclear dynamics, and solubility
Authors: Marcelli Marco , Stenoien David L. , Szafran Adam T. , Simeoni Silvia , Agoulnik Irina U. , Weigel Nancy L. , Moran Tim , Mikic Ivana , Price Jeffrey H. , Mancini Michael A.
Published: January 2006

Using manual and automated high throughput microscopy (HTM), ligand‐dependent trafficking of green fluorescent protein‐androgen receptor (GFP‐AR) was analyzed in fixed and living cells to determine its spatial distribution, solubility, mobility, and co‐activator interactions. Within minutes, addition of the agonist R1881 resulted translocation of GFP‐AR from the cytoplasm to the nucleus, where it displayed a hyperspeckled pattern and extraction resistance in low expressing cells. AR antagonists (Casodex, hydroxyflutamide) also caused nuclear translocation, however, the antagonist‐bound GFP‐AR had a more diffuse nuclear distribution, distinct from the agonist‐bound GFP‐AR, and was completely soluble; overexpressed GFP‐AR in treated cells was extraction resistant, independent of ligand type. To more dramatically show the different effects of ligand on AR distribution, we utilized an AR with a mutation in the DNA binding domain (ARC619Y) that forms distinct foci upon exposure to agonists but retains a diffuse nuclear distribution in the presence of antagonists. Live‐cell imaging of this mutant demonstrated that cytoplasmic foci formation occurs immediately upon agonist but not antagonist addition. Fluorescence recovery after photobleaching (FRAP) revealed that agonist‐bound GFP‐AR exhibited reduced mobility relative to unliganded or antagonist‐bound GFP‐AR. Importantly, agonist‐bound GFP‐AR mobility was strongly affected by protein expression levels in transiently transfected cells, and displayed reduced mobility even in slightly overexpressing cells. Cyan fluorescent protein‐AR (CFP‐AR) and yellow fluorescent protein‐CREB binding protein (YFP‐CBP) in the presence of agonists and antagonists were used to demonstrate that CFP‐AR specifically co‐localizes with YFP‐CBP in an agonist dependent manner. Dual FRAP experiments demonstrated that CBP mobility mirrored AR mobility only in the presence of agonist. HTM enabled simultaneous studies of the sub‐cellular distribution of GFP‐AR and ARC619Y in response to a range of concentrations of agonists and antagonists (ranging from 10−12 to 10−5) in thousands of cells. These results further support the notion that ligand specific interactions rapidly affect receptor and co‐factor organization, solubility, and molecular dynamics, and each can be aberrantly affected by mutation and overexpression. J. Cell. Biochem. 98: 770–788, 2006. © 2006 Wiley‐Liss, Inc.
Roles of MAP kinases in the regulation of bone matrix gene expressions in human osteoblasts by oscillatory fluid flow
Authors: Wu Chia‐Ching , Li Yi‐Shuan , Haga Jason H. , Wang Nanping , Lian Ian Y‐Z. , Su Fong‐Chin , Usami Shunichi , Chien Shu
Published: January 2006

We investigated the effects of oscillatory flow in regulating the gene expressions of type I collagen (COL1, the main component of human bone tissues) and osteopontin (OPN, the key gene for calcium deposition) in human osteoblast‐like (MG‐63) cells, and the roles of mitogen‐activated protein kinases (MAPKs) in this regulation. The cells were subjected to oscillatory flow (0.5 ± 4 dyn/cm2) or kept under static condition for various time periods (15 min, 30 min, 1 h, 2 h, 4 h, 8 h, and 16 h). Oscillatory flow caused significant up‐regulations of both COL1 and OPN gene expressions over the 16 h of study, and a transient activation of MAPKs was starting at 15 min and declining to basal level in 2 h. The flow‐induction of COL1 was blocked by an ERK inhibitor (PD98059) and reduced by a JNK inhibitor (SP600125), whereas that of OPN was abolished by PD98059. Analysis of the cis‐elements in the COL1 and OPN promoters suggests the involvement of transacting factors Elk‐1 and AP‐1 in the transcription regulation. The ERK inhibitor (PD98059) blocked Elk‐1 phosphorylation, as well as COL1 and OPN gene expression. The JNK inhibitor (SP600125) abolished c‐jun phosphorylation and COL1 expression. These results suggest that the flow‐induction of OPN was mediated through the ERK‐Elk1‐OPN pathway, and that COL1 was regulated by both the ERK‐Elk1‐COL1 and JNK‐c‐JUN‐COL1 pathway. J. Cell. Biochem. 98: 632–641, 2006. © 2006 Wiley‐Liss, Inc.
Hyperthermia engages the intrinsic apoptotic pathway by enhancing upstream caspase activation to overcome apoptotic resistance in MCF‐7 breast adenocarcinoma cells
Authors: Klostergaard J. , Leroux M.E. , Auzenne E. , Khodadadian M. , Spohn W. , Wu J.Y. , Donato N.J.
Published: January 2006

Febrile hyperthermia enhanced TNF‐stimulated apoptosis of MCF‐7 cells and overcame resistance in a TNF‐resistant, MCF‐7 variant (3E9), increasing their TNF‐sensitivity by 10‐ and 100‐fold, respectively. In either cell line, the hyperthermic potentiation was attributable to increased apoptosis that was totally quenched by caspase inhibition. In MCF‐7 cells, hyperthermic potentiation of apoptosis was associated with sustained activation of upstream caspases in response to TNF and more prominent engagement of the intrinsic apoptotic pathway. Apoptotic enhancement by hyperthermia was primarily mediated by caspase‐8 activation, as the specific inhibitor, Z‐IETD, blocked cell death, whereas direct engagement of the intrinsic apoptotic pathway (with doxorubicin) was not affected. In 3E9 cells, hyperthermia alone induced activation of caspase‐8, and was further enhanced by TNF. In 3E9 cells, hyperthermia caused TNF‐dependent loss of mitochondrial membrane potential and activation of capspase‐9 that was initiated and dependent on upstream caspases. MCF‐7 and 3E9 cells were equally sensitive to exogenous C6‐ceramide, but mass spectroscopic analysis of ceramide species indicated that total ceramide content was not enhanced by TNF and/or hyperthermia treatment, and that the combination of TNF and hyperthermia caused only modest elevation of one species (dihydro‐palmitoyl ceramide). We conclude that febrile hyperthermia potentiates apoptosis of MCF‐7 cells and overcomes TNF‐resistance by sustained activation of caspase‐8 and engagement of the intrinsic pathway that is independent of ceramide flux. This report provides the first evidence for regulation of caspase‐dependent apoptosis by febrile hyperthermia. J. Cell. Biochem. 98: 356–369, 2006. © 2006 Wiley‐Liss, Inc.
Probing membrane proteins using atomic force microscopy
Authors: Li Guangyong , Xi Ning , Wang Donna H.
Published: January 2006

To gain insights into how biological molecules function, advanced technologies enabling imaging, sensing, and actuating single molecules are required. The atomic force microscope (AFM) would be one of novel potential tools for these tasks. In this study, techniques and efforts using AFM to probe biomolecules are introduced and reviewed. The state‐of‐art techniques for characterizing specific single receptor using the functionalized AFM tip are discussed. An example of studying the angiotensin II type 1 (AT1) receptors expressed in sensory neuronal cells by AFM with a functionalized tip is given. Perspectives for identifying and characterizing specific individual membrane proteins using AFM in living cells are provided. Given that many diseases have their roots at the molecular scale and are best understood as a malfunctioning biological nanomachines, the prospects of these unique techniques in basic biomedical research or in clinical practice are beyond our imagination. J. Cell. Biochem. 97: 1191–1197, 2006. © 2006 Wiley‐Liss, Inc.
Fibroblast extracellular matrix gene expression in response to keratinocyte‐releasable stratifin
Authors: Ghaffari Abdi , Li Yunyaun , Karami Ali , Ghaffari Mazyar , Tredget Edward E. , Ghahary Aziz
Published: January 2006

Termination of wound‐healing process requires a fine balance between connective tissue deposition and its hydrolysis. Previously, we have demonstrated that keratinocyte‐releasable stratifin, also known as 14‐3‐3 σ protein, stimulates collagenase (MMP‐1) expression in dermal fibroblasts. However, role of extracellular stratifin in regulation of extracellular matrix (ECM) factors and other matrix metalloproteinases (MMPs) in dermal fibroblast remains unexplored. To address this question, large‐scale ECM gene expression profile were analyzed in human dermal fibroblasts co‐cultured with keratinocytes or treated with recombinant stratifin. Superarray pathway‐specific microarrays were utilized to identify upregulation or downregulation of 96 human ECM and adhesion molecule genes. RT‐PCR and Western blot were used to validate microarray expression profiles of selected genes. Comparison of gene profiles with the appropriate controls showed a significant (more than twofold) increase in expression of collagenase‐1, stromelysin‐1 and ‐2, neutrophil collagenase, and membrane type 5 MMP in dermal fibroblasts treated with stratifin or co‐cultured with keratinocytes. Expression of type I collagen and fibronectin genes decreased in the same fibroblasts. The results of a dose–response experiment showed that stratifin stimulates the expression of stromelysin‐1 (MMP‐3) mRNA by dermal fibroblasts in a concentration‐dependent fashion. Furthermore, Western blot analysis of fibroblast‐conditioned medium showed a peak in MMP‐3 protein levels 48 h following treatment with recombinant stratifin. In a lasting‐effect study, MMP‐3 protein was detected in fibroblast‐condition medium for up to 72 h post removal of stratifin. In conclusion, our results suggest that keratinocyte‐releasable stratifin plays a major role in induction of ECM degradation by dermal fibroblasts through stimulation of key MMPs, such as MMP‐1 and MMP‐3. Therefore, stratifin protein may prove to be a useful target for clinical intervention in controlling excessive wound healing in fibrotic conditions. J. Cell. Biochem. 98: 383–393, 2006. © 2006 Wiley‐Liss, Inc.
Prostanoid pattern and iNOS expression during chondrogenic differentiation of human mesenchymal stem cells
Authors: Mais Anna , Klein Thomas , Ullrich Volker , Schudt Christian , Lauer Gereon
Published: January 2006

Availability of human chondrocytes is a major limiting factor regarding drug discovery projects and tissue replacement therapies. As an alternative human mesenchymal stem cells (hMSCs) from bone marrow are taken into consideration as they can differentiate along the chondrogenic lineage. However, it remains to be shown whether they could form a valid model for primary chondrocytes with regards to inflammatory mediator production, like nitric oxide (NO) and prostanoids. We therefore investigated the production of NO and prostanoids in hMSCs over the course of chondrogenic differentiation and in response to IL‐1β using primary OA chondrocytes as reference. Chondrogenic differentiation was monitored over 28 days using collagen I, collagen II, and collagen X expression levels. Expression levels of inducible nitric oxide synthase (iNOS), levels of NO, and prostanoids were assessed using PCR, Griess assay, and GC/MS/MS, respectively. The hMSCs collagen expression profile during course of differentiation was consistent with a chondrocytic phenotype. Contrary to undifferentiated cells, differentiated hMSCs expressed iNOS and produced NO following stimulation with IL‐1β. Moreover, this induction of iNOS expression was corticosteroid insensitive. The spectrum of prostanoid production in differentiated hMSCs showed similarities to that of OA chondrocytes, with PGE2 as predominant product. We provide the first detailed characterization of NO and prostanoid production in hMSCs in the course of chondrogenic differentiation. Our results suggest that differentiated hMSCs form a valid model for chondrocytes concerning inflammatory mediator production. Furthermore, we propose that IL‐1β stimulation, leading to corticosteroid‐insensitive NO synthesis, can be used as a sensitive marker of chondrogenesis. J. Cell. Biochem. 98: 798–809, 2006. © 2006 Wiley‐Liss, Inc.
1α,25‐dihydroxyvitamin D3‐mediated stimulation of steroid sulphatase activity in myeloid leukaemic cell lines requires VDRnuc‐mediated activation of the RAS/RAF/ERK‐MAP kinase signalling pathway
Authors: Hughes Philip J. , Brown Geoffrey
Published: January 2006

1α,25‐dihydroxyvitamin D3 (1α,25(OH)2D3) stimulates the activity of steroid sulphatase (STS) in myeloid cells [Hughes et al., 2001, 2005]. This was attenuated by inhibitors of phospholipase D (PLD) (n‐butanol, 2,3‐diphosphoglyceric acid, C2‐ceramide) and phosphatidate phosphohydrolase (PAP) (propranolol and chlorpromazine), but was unaffected by inhibitors of phospholipase C. The 1α,25(OH)2D3‐induced STS activity was also attenuated by inhibitors of protein kinase Cα and protein kinase Cδ (Go 6976, HBDDE and rottlerin), but not by an inhibitor of protein kinase Cβ (LY379196). Additionally, 1α,25(OH)2D3‐induced STS activity was attenuated by inhibitors of RAS (manumycin A), RAF (GW5074), MEK (PD098059 and U1026) and JNK (SP600125), but not p38 (PD169316). 1α,25(OH)2D3 produced a rapid and long lasting stimulation of the ERK‐MAP kinase signalling cascade in HL60 myeloid leukaemic cells. This ‘non‐genomic’ effect of 1α,25(OH)2D3 blocked by pharmacological antagonists of nuclear vitamin D receptors (VDRnuc) and does not appear to require hetero‐dimerisation with the retinoid‐X receptor (RXR). Inhibitors of the Src tyrosine kinase (PP1), RAS (manumycin A), RAS–RAF interactions (sulindac sulphide and RAS inhibitory peptide), RAF (GW5074 or chloroquine), and protein kinase Cα (HBDDE) abrogated the 1α,25(OH)2D3‐stimulated increase in ERK‐MAP kinase activity. Taken together, these results show that 1α,25(OH)2D3/VDRnuc activation of the RAS/RAF/ERK‐MAP kinase signalling pathway plays an important role in augmenting STS activity in human myeloid leukaemic cell lines. J. Cell. Biochem. 98: 590–617, 2006. � 2006 Wiley‐Liss, Inc.
Lysyl oxidase regulates actin filament formation through the p130Cas/Crk/DOCK180 signaling complex
Authors: Payne Stacey L. , Hendrix Mary J.C. , Kirschmann Dawn A.
Published: January 2006

We have previously demonstrated that lysyl oxidase (LOX) is expressed in invasive breast cancer cells compared to poorly invasive cells. Additionally, we have recently shown that LOX regulates cell migration, a key step in the invasion process, through a hydrogen peroxide‐dependent mechanism involving the focal adhesion kinase (FAK)/Src signaling complex. Here we further elucidate the role of LOX in cell motility/migration by examining the role of LOX in actin filament polymerization. We demonstrate that inhibition of LOX leads to an increase in phalloidin staining, directly associated with an increase in actin stress fiber formation. This increase in staining was confirmed by activity assays showing an increase in Rho activity with decreased LOX activity. Additionally, Rac and Cdc42 activity decreased with the reduction in LOX activity. Taken together, these data demonstrate a loss of a motogenic phenotype with decreased LOX activity. Finally, in order to elucidate the mechanism by which LOX regulates actin polymerization, we have demonstrated that LOX facilitates p130Cas phosphorylation, which allows for the binding to CAS related kinase (Crk) and formation of the p130Cas/Crk/DOCK180 signaling complex. Formation of this complex leads to an increase in Rac‐GTP, which decreases actin stress fiber formation and increases formation of lamellipodium. These data demonstrate that LOX regulates cell motility/migration through changes in actin filament polymerization, which involve the regulation of the p130Cas/Crk/DOCK180 signaling pathway. Elucidating the role of LOX in the regulation of cell motility will allow the development of more effective therapeutic strategies to treat invasive/metastatic breast cancer. J. Cell. Biochem. 98: 827–837, 2006. © 2006 Wiley‐Liss, Inc.
Salvianolic acid B attenuates cyclooxygenase‐2 expression in vitro in LPS‐treated human aortic smooth muscle cells and in vivo in the apolipoprotein‐E‐deficient mouse aorta
Authors: Chen Yuh‐Lien , Hu Cing‐Siang , Lin Feng‐Yen , Chen Yung‐Hsiang , Sheu Li‐Min , Ku Hung‐Hai , Shiao Ming‐Shi , Chen Jaw‐Wen , Lin Shing‐Jong
Published: January 2006

Inflammation plays an essential role in atherosclerosis and post‐angioplasty restenosis and the synthesis and release of inflammatory cytokines from vascular smooth muscle cells is an important contributor to these pathologies. It is assumed that drugs that prevent the overproduction of inflammatory cytokines may inhibit cardiovascular disorders. In the present study, the effects of a water‐soluble antioxidant, salvianolic acid B (Sal B), derived from a Chinese herb, on the expression of cyclooxygenase (COX) in lipopolysaccharide (LPS)‐treated human aortic smooth muscle cells (HASMCs) and in the aortas of cholesterol‐fed apoE deficient mice were investigated. In unstimulated HASMCs, COX‐2 mRNA and protein were almost undetectable, but were strongly upregulated in response to LPS. In contrast, HASMCs with or without LPS treatment showed constitutive expression of COX‐1 mRNA and protein. The activation of COX‐2 protein synthesis in LPS‐stimulated HASMCs was shown to involve the activation of the extracellular‐signal‐regulated kinase 1/2 (ERK1/2), c‐Jun NH2‐terminal kinase (JNK), and p38 mitogen‐activated protein kinase pathway. Incubation of HASMCs with Sal B before LPS stimulation resulted in pronounced downregulation of COX‐2 expression. Sal B treatment suppressed ERK1/2 and JNK phosphorylation and attenuated the increase in prostaglandin E2 production and NADPH oxidase activity in LPS‐treated HASMCs. When apoE‐deficient mice were fed a 0.15% cholesterol diet with or without supplementation with 0.3% Sal B for 12 weeks, the intima/media area ratio in the thoracic aortas was significantly reduced in the Sal B group (0.010 ± 0.009%) compared to the apoE‐deficient group (0.114 ± 0.043%) and there was a significant reduction in COX‐2 protein expression in the thickened intima. These results demonstrate that Sal B has anti‐inflammatory properties and may explain its anti‐atherosclerotic properties. This new mechanism of action of Sal B, in addition to its previously reported inhibition of LDL oxidation, may help explain its efficacy in the treatment of atherosclerosis. J. Cell. Biochem. 98: 618–631, 2006. © 2006 Wiley‐Liss, Inc.
Engineered nanoparticles as precise drug delivery systems
Authors: Yih T.C. , Al‐Fandi M.
Published: January 2006

With the remarkable development of nanotechnology in recent years, new drug delivery approaches based on the state‐of‐the‐art nanotechnology have been receiving significant attention. Nanoparticles, an evolvement of nanotechnology, are increasingly considered as a potential candidate to carry therapeutic agents safely into a targeted compartment in an organ, particular tissue or cell. These particles are colloidal structures with a diameter smaller than 1,000 nm, and therefore can penetrate through diminutive capillaries into the cell's internal machinery. This innovative delivery technique might be a promising technology to meet the current challenges in drug delivery. When loaded with a gene or drug agent, nanoparticles can become nanopills, which can effectively treat problematical diseases such as cancer. This article summarizes different types of nanoparticles drug delivery systems under investigation and their prospective therapeutic applications. Also, this article presents a closer look at the advances, current challenges, and future direction of nanoparticles drug delivery systems. J. Cell. Biochem. 97: 1184–1190, 2006. © 2006 Wiley‐Liss, Inc.
Functional characterization of hNUDC as a novel accumulator that specifically acts on in vitro megakaryocytopoiesis and in vivo platelet production
Authors: Wei Ming‐Xu , Yang Yan , Ge Yi‐Chen , Xu Peilin
Published: January 2006

Human NUDC (hNUDC) has been previously described as a human homolog of a fungal nuclear migration protein. It is a multifunctional interactive protein that forms an association with the microtubule motor complex in a variety of cells. Our recent studies demonstrated that hNUDC could bind specifically to the thrombopoietin receptor (Mpl) and suggest a potential role for hNUDC in megakaryocytopoiesis and thrombopoiesis. The present study is designed to define its biological activity. We demonstrate that the recombinant hNUDC significantly increases megakaryocyte maturation in serum‐free liquid‐cultured human CD34+ cells and stimulates colony formation in serum‐free semi‐solid cultures. Flow cytometry analyses also confirm the stimulatory effect of hNUDC on megakaryocyte polyploidization and in vitro platelet production. In vivo experiments further demonstrate that the administration of hNUDC substantially enhance the number of circulating platelets in normal mice. J. Cell. Biochem. 98: 429–439, 2006. © 2006 Wiley‐Liss, Inc.
LDL induces Saos2 osteoblasts death via Akt pathways responsive to a neutral sphingomyelinase inhibitor
Authors: Klein Benjamin Y. , Kerem Zohar , Rojansky Nathan
Published: January 2006

Atherosclerosis is epidemiologically associated with postmenopausal osteoporosis (OP) presumably by common etiologic factors, reflecting a state of co‐morbidity in aging. Osteoblasts make a significant facet of this co‐morbidity state. Since oxidized low‐density lipoprotein (oxLDL) is a major factor in generation of vascular wall pathology, we examined the ability of native LDL (nLDL) and oxLDL to induce Saos2 osteoblasts growth arrest. OxLDL induced Saos2 cell death with morphological features of apoptosis that was inhibited mainly by caspase‐9 and partially by caspase‐3 but not by caspase‐8 inhibitors. nLDL, like oxLDL, has induced cell death, where 60% (P = 0.00033) and 30% (P = 0.075, ns) of the cell death, respectively, could be inhibited by scyphostatin (a neutral sphingomyelinase [nSMase] inhibitor). Upon similar condition, nLDL inhibited the phosphorylation of Akt and two of its downstream targets, fork head receptor (FKHR) and glycogen synthase kinase‐3 (GSK3). This is a pathway that stimulates cell survival and proliferation. nLDL has also induced an increase in the proapoptotic Bcl‐Xs and it has diminished the potential antiapoptotic Src kinase activity. At the 4 h time‐point, upon a substantial decrease in nLDL‐induced Akt phosphorylation, scyphostatin has inhibited the reduction in FKHR and GSK3 phosphorylation but inexplicably not that of Akt. Scyphostatin has also corrected the reduction in Src kinase activity. Taken together, the results indicate that nLDL has induced apoptosis in Saos2 osteoblasts by inactivation of the pathway downstream to Akt using nSMase, and by involvement of Src kinase. Inferring that caspase‐9 was the main executioner (rather than caspase‐8 and‐3) in Saos2 cell death, indicates that the nSMase‐induced release of ceramide, directly activated the intrinsic mitochondrial apoptotic pathway. With regard to the Akt inactivation by nLDL, Saos2 osteoblasts responded in an opposite fashion to the response reported by others, in macrophages. J. Cell. Biochem. 98: 661–671, 2006. © 2006 Wiley‐Liss, Inc.
CCN2, connective tissue growth factor, stimulates collagen deposition by gingival fibroblasts via module 3 and α6‐ and β1 integrins
Authors: Heng Edwin C.K. , Huang Yuanyi , Black Samuel A. , Trackman Philip C.
Published: January 2006

CCN2, (connective tissue growth factor, CTGF) is a matricellular factor associated with fibrosis that plays an important role in the production and maintenance of fibrotic lesions. Increased collagen deposition and accumulation is a common feature of fibrotic tissues. The mechanisms by which CCN2/CTGF contributes to fibrosis are not well understood. Previous studies suggest that CTGF exerts some of its biological effects at least in part by integrin binding, though this mechanism has not been previously shown to contribute to fibrosis. Utilizing full length CCN2/CTGF, CCN2/CTGF fragments, and integrin neutralizing antibodies, we provide evidence that the effects of CCN2/CTGF to stimulate extracellular matrix deposition by gingival fibroblasts are mediated by the C‐terminal half of CCN2/CTGF, and by α6 and β1 integrins. In addition, a synthetic peptide corresponding to a region of CCN2/CTGF domain 3 that binds α6β1 inhibits the collagen‐deposition assay. These studies employed a new and relatively rapid assay for CCN2/CTGF‐stimulated collagen deposition based on Sirius Red staining of cell layers. Data obtained support a pathway in which CCN2/CTGF could bind to α6β1 integrin and stimulate collagen deposition. These findings provide new experimental methodologies applicable to uncovering the mechanism and signal transduction pathways of CCN2/CTGF‐mediated collagen deposition, and may provide insights into potential therapeutic strategies to treat gingival fibrosis and other fibrotic conditions. J. Cell. Biochem. 98: 409–420, 2006. © 2006 Wiley‐Liss, Inc.
Collagen type I selectively activates ectodomain shedding of the discoidin domain receptor 1: Involvement of Src tyrosine kinase
Authors: Slack Barbara E. , Siniaia Marina S. , Blusztajn Jan K.
Published: January 2006

The discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase that is highly expressed in breast carcinoma cells. Upon binding to collagen, DDR1 undergoes autophosphorylation followed by limited proteolysis to generate a tyrosine phosphorylated C‐terminal fragment (CTF). Although it was postulated that this fragment is formed as a result of shedding of the N‐terminal ectodomain, collagen‐dependent release of the DDR1 extracellular domain has not been demonstrated. We now report that, in conjunction with CTF formation, collagen type I stimulates concentration‐dependent, saturable shedding of the DDR1 ectodomain from two carcinoma cell lines, and from transfected cells. In contrast, collagen did not promote cleavage of other transmembrane proteins including the amyloid precursor protein (APP), ErbB2, and E‐cadherin. Collagen‐dependent tyrosine phosphorylation and proteolysis of DDR1 in carcinoma cells were reduced by a pharmacologic Src inhibitor. Moreover, expression of a dominant negative Src mutant protein in human embryonic kidney cells inhibited collagen‐dependent phosphorylation and shedding of co‐transfected DDR1. The hydroxamate‐based metalloproteinase inhibitor TAPI‐1 (tumor necrosis factor‐α protease inhibitor‐1), and tissue inhibitor of metalloproteinase (TIMP)‐3, also blocked collagen‐evoked DDR1 shedding, but did not reduce levels of the phosphorylated CTF. Neither shedding nor CTF formation were affected by the γ‐secretase inhibitor, L‐685,458. The results demonstrate that collagen‐evoked ectodomain cleavage of DDR1 is mediated in part by Src‐dependent activation or recruitment of a matrix‐ or disintegrin metalloproteinase, and that CTF formation can occur independently of ectodomain shedding. Delayed shedding of the DDR1 ectodomain may represent a mechanism that limits DDR1‐dependent cell adhesion and migration on collagen matrices. J. Cell. Biochem. 98: 672–684, 2006. © 2006 Wiley‐Liss, Inc.
Role of amino acids in translational mechanisms governing milk protein synthesis in murine and ruminant mammary epithelial cells
Authors: Moshel Yana , Rhoads Robert E. , Barash Itamar
Published: January 2006

The role of amino acids (AA) on translational regulation in mammary epithelial cells cultured under lactogenic conditions was studied. The rates of total protein synthesis and β‐lactoglobulin (BLG) synthesis in mouse CID‐9 cells were 2.1‐ or 3.1‐fold higher, respectively, than in their bovine L‐1 counterparts. Total AA deprivation or selective deprivation of Leu had a negative protein‐specific effect on BLG synthesis that was more pronounced in bovine cells than in murine cells. Dephosphorylation of eukaryotic initiation factor 4E‐binding protein 1 (4E‐BP1) and S6 kinase (S6K1) on Thr389 but not on Ser411 was also more prominent in bovine cells. Noteably, deprivation of Leu had a less marked effect on BLG synthesis and 4E‐BP1 or S6K1 phosphorylation than deprivation of all AA. In AA‐deprived CID‐9 cells, Leu specifically restored BLG synthesis from pre‐existing mRNA whereas AA also restored total protein synthesis. This restoration was associated with a more pronounced effect on 4E‐BP1 and S6K1 phosphorylation in bovine versus murine cells. Rapamycin specifically reduced Leu‐ and AA‐stimulated BLG translation initiation in a dose‐dependent manner. A further reduction was observed for Leu‐treated cells in the presence of LY294002, a PI3K (phosphatidylinositol 3‐kinase) inhibitor, which also reduced total protein synthesis. These findings suggest that direct signaling from AA to the translational machinery is involved in determining the rates of milk protein synthesis in mammary epithelial cells. J. Cell. Biochem. 98: 685–700, 2006. © 2006 Wiley‐Liss, Inc.
Dual involvement of protein kinase C δ in apoptosis induced by syndecan‐2 in osteoblasts
Authors: Orosco Armelle , Fromigué Olivia , Haÿ Eric , Marie Pierre J. , Modrowski Dominique
Published: January 2006

Syndecans are proteoglycans that act as signaling molecules. Previously, we showed that syndecan‐2 (SYND2) is involved in the control of osteoblastic (OB) cell apoptosis. Here, we show a novel functional interaction between SYND2 and protein kinase C δ (PKCδ). Overexpression of SYND2 in MG63 OB cells resulted in increased PKCδ protein level without change in PKCδ mRNA production. In SYND2‐transfected cells, the increase in PKCδ was restricted to the cytosolic compartment, threonine 505‐PKCδ was underphosphorylated and immunoprecipitated PKCδ showed decreased capacity to phosphorylate histone, indicating that SYND2 decreased PKCδ activity. Inhibition of PKCδ by Rottlerin or a dead‐kinase dominant negative (DN) construct activated effector caspases and increased the number of apoptotic cells. In addition, rescue of kinase activity with a construct coding, the PKCδ catalytic domain (CAT) reduced SYND2‐induced apoptosis. This indicates that PKCδ acts as a pro‐survival kinase and that SYND2 inhibits the anti‐apoptotic action of PKCδ in OB cells. We also showed that overexpression of PKCδ wild type (WT) induced osteoblast apoptosis. Moreover, inhibition of PKCδ by siRNA resulted in increased apoptosis in control cells but reduced apoptosis in SYND2‐overexpressing osteoblasts, indicating that SYND2 requires PKCδ accumulation to induce apoptosis. These results show that SYND2 modulates PKCδ actions by inhibition of the canonical allosterical activation pathway that plays an anti‐apoptotic role in OB cells, and promotion of a pro‐apoptotic role that may depend on PKCδ protein level and that participates to the induction of cell death by SYND2. This establishes a functional interaction between SYND2 and PKCδ in osteoblasts. J. Cell. Biochem. 98: 838–850, 2006. © 2006 Wiley‐Liss, Inc.
Recovery of nineteenth‐century Tokyo/Osaka meteorological data in Japan
Authors: Zaiki M. , Können G. P. , Tsukahara T. , Jones P. D. , Mikami T. , Matsumoto K.
Published: January 2006

We have recovered instrumental temperature and pressure observations from Tokyo covering the periods 1825–1828, 1839–1855, and 1872–1875; from Yokohama covering the periods 1860–1871 and 1874; from Osaka covering the periods 1828–1833 and 1869–1871; and from Kobe covering the periods 1869–1871 and 1875–1888. The newly recovered records contain data before the 1870s, which is a period where, until recently, no instrumental data in Japan were believed to exist. Their addition to the previous backward extension of Japanese series, as based on the recently recovered intermittent Dejima/Nagasaki series 1819–1878, implies that the nineteenth‐century extension of the Japanese instrumental record no longer contains major temporal gaps. The recovered data were used for a preliminary calculation of the west‐Japan temperature (WJT) series, which is a representative temperature series for the area. The existence of a warm epoch in the 1850s over W‐Japan and a downward temperature trend till the early twentieth century, as previously inferred from documentary data, is confirmed from the WJT data. The pressure data implies that the temperature differences between the nineteenth and twentieth centuries are at least partly caused by a change in atmospheric circulation. Copyright © 2006 Royal Meteorological Society.
Synoptic climatological influences on the spatial and temporal variability of aerosols over North America
Authors: Power Helen C. , Sheridan Scott C. , Senkbeil Jason C.
Published: January 2006

The spatial and temporal variability of atmospheric aerosols is not well understood, as most studies have been constrained to data sets that include few stations and are of short duration. Furthermore, all methods for quantifying atmospheric turbidity suffer from a major constraint in that they require cloudless sky conditions. This restriction produces gaps in the turbidity record and sampling bias, which has led to questionable inferences about the variability of aerosols.

In this research, we address these concerns via analyses at scales broader than all previous studies. We analyzed the spectral aerosol optical depth at 500 nm (τa5) and Ångström's wavelength exponent (α), which represents the relative size distribution of aerosols. A total of 27 sites, with a mean period of record of 7.3 years, are included. Beyond seasonal and spatial summaries of aerosol variability, we have divided observations by synoptic condition, utilizing the Spatial Synoptic Classification (SSC).

Our results show that atmospheric turbidity across North America is greatest over the east. Seasonality of both parameters was shown, most notably a greater τa5 during summertime. Utilizing the SSC, we have uncovered significant differences across weather types. Moist weather types, especially moist tropical, display considerably higher turbidity, while the colder, drier dry polar weather type is associated with low aerosol optical depth. Certain weather types show considerable seasonal variability; the dry tropical weather type is associated with relatively low values in winter, but high values in summer, when convection is significant. Cluster analyses of stations yielded three general regions, each with similar synoptic variability: a western cluster with low aerosol optical depth and minimal synoptic variability, an eastern cluster with higher turbidity and variability, and a cluster located on the periphery of the eastern cluster, associated with moderate levels of turbidity but very high variability, suggesting a varied influence of nearby industrial areas. Copyright © 2006 Royal Meteorological Society.
Modelling current trends in Northern Hemisphere temperatures
Authors: Mills Terence C.
Published: January 2006

Fitting a trend is of interest in many disciplines, but it is of particular importance in climatology, where estimating the current and recent trend in temperature is thought to provide a major indication of the presence of global warming. A range of ad hoc methods of trend fitting have been proposed, with little consensus as to the most appropriate techniques to use. The aim of this paper is to consider a range of trend extraction techniques, none of which require ‘padding’ out the series beyond the end of the available observations, and to use these to estimate the trend of annual mean Northern Hemisphere (NH) temperatures. A comparison of the trends estimated by these methods thus provides a robust indication of the likely range of current trend temperature increases and hence inform, in a timely quantitative fashion, arguments based on global temperature data concerning the nature and extent of global warming and climate change. For the complete sample 1856–2003, the trend is characterised as having long waves about an underlying increasing level. Since around 1970, all techniques display a pronounced warming trend. However, they also provide a range of trend functions so that extrapolation far into the future would be a hazardous exercise. Copyright © 2006 Royal Meteorological Society.
Projecting the risk of future climate shifts
Authors: Enfield David B. , Cid‐Serrano Luis
Published: January 2006

Recent research has shown that decadal‐to‐multidecadal (D2M) climate variability is associated with environmental changes that have important consequences for human activities, such as public health, water availability, frequency of hurricanes, and so forth. As scientists, how do we convert these relationships into decision support products useful to water managers, insurance actuaries, and others, whose principal interest lies in knowing when future climate regime shifts will likely occur that affect long‐horizon decisions? Unfortunately, numerical models are far from being able to make deterministic predictions for future D2M climate shifts. However, the recent development of paleoclimate reconstructions of the Atlantic Multidecadal Oscillation (AMO) (Gray et al., 2004) and Pacific Decadal Oscillation (PDO); (MacDonald and Case, 2005) give us a viable alternative: to estimate probability distribution functions from long climate index series that allow us to calculate the probability of future D2M regime shifts. In this paper, we show how probabilistic projections can be developed for a specific climate mode—the AMO as represented by the Gray et al. (2004) tree‐ring reconstruction. The methods are robust and can be applied to any D2M climate mode for which a sufficiently long index series exists, as well as to the growing body of paleo‐proxy reconstructions that have become available. The target index need not be a paleo‐proxy calibrated against a climate index; it may profitably be calibrated against a specific resource of interest, such as stream flow or lake levels. Copyright © 2006 Royal Meteorological Society