bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anchoring of Ru–Pt and Ru–Au Clusters onto a Phosphane‐Functionalized Carbon Support
Authors: Willocq Christopher , Vidick Deborah , Tinant Bernard , Delcorte Arnaud , Bertrand Patrick , Devillers Michel , Hermans Sophie 
Published: September 2011

AbstractTwo mixed‐metal clusters, [Ru5PtC(CO)14(COD)] (1) and [Ru6Au2C(CO)16(PPh3)2] (2), were anchored onto a prefunctionalized active carbon support (C) with chelating phosphane groups on its surface. These clusters were also deposited onto the unmodified support (CSX+) for comparison. The incorporation of 1 and 2 on both supports was studied by a combination of SIMS and XPS. When the clusters were anchored onto the functionalized carbon support, SIMS spectra displayed characteristic patterns that were different from those obtained in the case of their deposition on the unmodified support. In the latter case, spectra corresponded to the results obtained with pure unsupported clusters. XPS analyses of the supported species seemed to indicate that the stoichiometry of the clusters was retained after anchoring and that their dispersion was better on C than on CSX+. This indicates that the phosphanes act as anchors for noble metal compounds through a ligand exchange mechanism. The supported samples were then thermally activated and characterized by SIMS, XPS, TEM/EDXS and XRD. Analyses by SIMS showed that the cluster ligand shell was removed during thermal treatment. XPS measurements indicated that the composition of the supported particles corresponded to that of the starting clusters and that the dispersion remained higher in the case of C. Well‐dispersed bimetallic‐supported nanoparticles (1–2 nm) were obtained when cluster 1 was used as the precursor, whereas anchoring of cluster 2 resulted in its fragmentation leading to supported nanoparticles of variable stoichiometries. Reactions with soluble model molecules were carried out to prove the chemical bonding of 1. Crystallization of the new cluster [Ru5PtC(CO)14{(PPh2CH2)2NC3H7}] confirmed the chemical bonding of cluster 1 onto the C support through a ligand exchange mechanism involving COD.
One‐Pot Synthesis of Core‐Shell Silver‐Gold Nanoparticle Solutions and Their Interaction with Methylene Blue Dye
Authors: Uppal Madeeha A. , Ewing Michael B. , Parkin Ivan P. 
Published: September 2011

AbstractA one‐pot modified Turkevich synthesis was used to synthesise a range of colloids from pure Ag, through Ag/Au core‐shell mixtures to pure Au by the thermal co‐addition of trisodium citrate to auric acid and silver nitrate mixtures. The colloids were analysed by means of XRD and wide‐beam energy dispersive X‐ray (EDX) analysis. The UV/Vis spectroscopy showed a non‐linear variation in the surface plasmon resonance band with the Au/Ag ratio, consistent with core‐shell formation. High resolution transmission electron microscopy (HRTEM) imaging, in conjunction with thin‐beam EDX line analysis, confirmed the presence of predominantly Ag cores and Au exteriors in the Au/Ag mixture. The argon ion sputtering with X‐ray photoelectron spectroscopy (XPS) measurements of the particles also indicated a Ag‐Au core‐shell formation. Ag0, Au0 and significant levels of AuI states were observed, which correlate with a Ag‐Au core‐shell model where the gold shell becomes partially oxidised at the surface. The subsequent titration of the colloids with methylene blue (MB) dye showed strong positive increases in the extinction coefficient at the absorption maximum. At the optimum levels of dye addition, a linear relationship was found between the average nanoparticle size and the number of dye solvation shells. The pure Au and Ag colloids showed the greatest propensity for an increase in the extinction coefficient of MB due to an enhanced transfer of the surface plasmons to the localised dye molecules and demonstrated the potential for increased functionality as light‐activated agents in the lethal photosensitisation of bacteria.
Coordination and Catalytic Activity of Ruthenium Complexes Containing Tridentate P,N,O Ligands
Authors: Lee Chun‐Chin , Chu Wan‐Yi , Liu Yi‐Hong , Peng Shie‐Ming , Liu Shiuh‐Tzung 
Published: September 2011

AbstractThe coordination chemistry of RuII ions with [2‐(diphenylphosphanyl)‐N‐(o‐hydroxybenzylidene)]aniline (PNO‐H) and the methylated analogue PNO‐Me have been studied. Thus, [(PNO)RuCl(dmso)2] (1), [(PNO)2Ru] (2), [(PNO)RuCl(PPh3)] (3) and [(PNO)RuCl(CO)2] (4) were synthesized by reactions of various RuII precursors with PNO‐H. Treatment of PNO‐Me with [RuCl2(dmso)4] resulted in in the formation of [P,N‐(PNO‐Me)Ru(dmso)2Cl2] (5). However, complexation of PNO‐Me with [RuCl2(CO)3(THF)] (THF = tetrahydrofuran) provided a mixture of [P,N‐(PNO‐Me)Ru(CO)2Cl2] (6) and 4 because O‐demethylation took place during the reaction. All of the RuII complexes have been characterized by elemental analysis and spectroscopic techniques, as well as X‐ray crystal structural analysis for 2, 4 and 6. The ruthenium complexes investigated in this work, except 2, are good precatalysts for the reductive amination of amine with alcohols, and 4 appears to be the best. Moreover, 4 can catalyze the direct amination of nitrobenzene with benzyl alcohol to the corresponding secondary amine.
Beneficial compaction of spinal cord lesion by migrating astrocytes through glycogen synthase kinase‐3 inhibition
Authors: Renault‐Mihara Francois , Katoh Hiroyuki , Ikegami Takeshi , Iwanami Akio , Mukaino Masahiko , Yasuda Akimasa , Nori Satoshi , Mabuchi Yo , Tada Hirobumi , Shibata Shinsuke , Saito Ken , Matsushita Masayuki , Kaibuchi Kozo , Okada Seiji , Toyama Yoshiaki , Nakamura Masaya , Okano Hideyuki 
Published: September 2011

AbstractThe migratory response of astrocytes is essential for restricting inflammation and preserving tissue function after spinal cord injury (SCI), but the mechanisms involved are poorly understood. Here, we observed stimulation of in vitro astrocyte migration by the new potent glycogen synthase kinase‐3 (GSK‐3) inhibitor Ro3303544 and investigated the effect of Ro3303544 administration for 5 days following SCI in mice. This treatment resulted in accelerated migration of reactive astrocytes to sequester inflammatory cells that spared myelinated fibres and significantly promoted functional recovery. Moreover, the decreased extent of chondroitin sulphate proteoglycans and collagen IV demonstrated that scarring was reduced in Ro3303544‐treated mice. A variety of in vitro and in vivo experiments further suggested that GSK‐3 inhibition stimulated astrocyte migration by decreasing adhesive activity via reduced surface expression of β1‐integrin. Our results reveal a novel benefit of GSK‐3 inhibition for SCI and suggest that the stimulation of astrocyte migration is a feasible therapeutic strategy for traumatic injury in the central nervous system.
Local variations of solifluction activity and environment in the Abisko Mountains, Northern Sweden
Authors: Ridefelt Hanna , Boelhouwers Jan , Etzelmüller Bernd 
Published: September 2011

ABSTRACTSeven sites within the mountain region of Abisko, northern Sweden, were selected for measurement of solifluction movement rates and correlation with the local environmental factors. Grids with sizes from 20 m × 30 m to 50 m × 100 m included both solifluction landforms and adjacent ground. Positions of movement markers and the terrain were recorded and the grid areas were digitally reconstructed. This allowed topography, vegetation and soil texture (fraction of fine material) surfaces to be interpolated and used together with data on soil moisture in statistical analyses. Significant correlations differ from site to site indicating that environmental factors have varying importance and inter‐relations depending on the local setting. Geomorphic work was also assessed within the grids. The results indicate measurable geomorphic work where no landforms are present. These areas may make larger contributions to sediment displacement than where solifluction landforms exist. Solifluction is an important denudational agent in the region and has its greatest impact on landscape development in the western part of the region. Copyright © 2011 John Wiley & Sons, Ltd.
Dynamic motility of microglia: Purinergic modulation of microglial movement in the normal and pathological brain
Authors: Ohsawa Keiko , Kohsaka Shinichi 
Published: September 2011

AbstractMicroglia have highly branched and motile cell processes and constantly screen the brain parenchyma under physiological conditions. In response to pathological stimuli, microglia exhibit morphological changes and migrate toward the lesioned site, where they play important roles in inflammatory reactions and neuronal damage. Within minutes of brain damage, microglial processes rapidly extend toward the injured site. The chemoattractive response is triggered by ATP released at the site of injury and the consequent activation of the purinergic receptor P2Y12R on microglia. In addition to the purinergic signals, various neuronal signaling molecules actively and negatively control microglial motility, which is important for regulating the functional activation of microglia in response to pathology. In this review, we focus on the dynamic motion of microglia and describe several key molecules regulating microglial motility in normal and pathological brain tissues. © 2011 Wiley‐Liss, Inc.
Expression and regulation of AC133 and CD133 in glioblastoma
Authors: Campos Benito , Zeng Lingcheng , DaoTrong Philip H. , Eckstein Volker , Unterberg Andreas , Mairbäurl Heimo , Herold‐Mende Christel 
Published: September 2011

AbstractThe biological significance of CD133 in glioblastoma is controversial. Above all, there is disagreement concerning the proper approach, the appropriate (cell) model and the suitable microenvironment to study this molecule, often leading to inconsistent experimental results among studies. In consideration of a primary need to dissect and to understand the CD133 phenotype in glioblastoma we performed a comprehensive analysis of CD133 expression and regulation in a large set of glioblastoma cell lines (n = 20) as well as in tumor xenografts. Our analysis considered alternatively spliced mRNA transcripts, different protein epitopes as well as varying sub‐cellular localizations of CD133 and explored its regulation under pertinent micro‐environmental conditions. CD133 mRNA and CD133 protein could be detected in all relevant types of glioblastoma cell lines. In addition, we detected frequent intracellular CD133 protein accumulations located to the ER and/or Golgi apparatus but seemingly unrelated to particular CD133 splice variants or protein epitopes. In contrast, membrane‐bound expression of CD133 was restricted to tumor cells bearing the extracellular CD133 epitope AC133. Only in these cells, differentiation and oxygen levels clearly impacted on AC133 expression and to some extent also influenced CD133 mRNA and protein expression. Most importantly, however, modulation of AC133 levels could occur independently of changes in CD133 mRNA transcription, CD133 protein translation, protein retention or protein shedding. Our results suggest that the AC133 epitope, rather than CD133 mRNA or protein, mirrors malignancy‐related tumor traits such as tumor differentiation and local oxygen tension levels, and thus corroborate its role as a biologically relevant cancer marker. © 2011 Wiley‐Liss, Inc.
Nitric oxide induces the expression of the monocarboxylate transporter MCT4 in cultured astrocytes by a cGMP‐independent transcriptional activation
Authors: Marcillac Fabrice , Brix Britta , Repond Cendrine , Jöhren Olaf , Pellerin Luc 
Published: September 2011

AbstractThe monocarboxylate transporter MCT4 is a proton‐linked carrier particularly important for lactate release from highly glycolytic cells. In the central nervous system, MCT4 is exclusively expressed by astrocytes. Surprisingly, MCT4 expression in primary cultures of mouse cortical astrocytes is conspicuously low, suggesting that an external, nonastrocytic signal is necessary to obtain the observed pattern of expression in vivo. Here, we demonstrate that nitric oxide (NO), delivered by various NO donors, time‐ and dose‐dependently induces MCT4 expression in cultured cortical astrocytes both at the mRNA and protein levels. In contrast, NO does not enhance the expression of MCT1, the other astrocytic monocarboxylate transporter. The transcriptional effect of NO is not mediated by a cGMP‐dependent mechanism as shown by the absence of effect of a cGMP analog or of a selective guanylate cyclase inhibitor. NO causes an increase in astrocytic lactate transport capacity which requires the enhancement of MCT4 expression as both are prevented by the use of a specific siRNA against MCT4. In addition, cumulated lactate release by astrocytes over a period of 24 h was also enhanced by NO treatment. Our data suggest that NO represents a putative intercellular signal to control MCT4 expression in astrocytes and in doing so, to facilitate lactate transfer to other surrounding cell types in the central nervous system. © 2011 Wiley‐Liss, Inc.
Heat and mass transfer effects on peristaltic flow of an Oldroyd‐B fluid in a channel with compliant walls
Authors: Hayat T. , Hina S. , Hendi Awatif A. 
Published: September 2011

AbstractThis investigation describes the peristaltic motion of a magnetohydrodynamic (MHD) Oldroyd‐B fluid with heat and mass transfer. An incompressible Oldroyd‐B fluid is considered in a channel with flexible walls. The relevant equations are developed by employing equations of continuity, momentum, energy, and concentration. Expressions of stream function, temperature, concentration field, and heat transfer coefficient are presented when the wave number is small. The obtained solutions are graphically discussed for the several interesting parameters entering into the problem. It is found that relaxation and retardation times have opposite effects on the size of the trapped bolus. © 2011 Wiley Periodicals, Inc. Heat Trans Asian Res; Published online in Wiley Online Library (wileyonlinelibrary.com/journal/htj). DOI 10.1002/htj.20380
Boundary layer flow of an Oldroyd‐B fluid with convective boundary conditions
Authors: Hayat T. , Iqbal Z. , Mustafa M. , Obaidat S. 
Published: September 2011

AbstractThis study is presented for the flow of an Oldroyd‐B fluid subject to convective boundary conditions. The two‐dimensional equations are simplified by using boundary layer approximations. The analytic solutions in the whole spatial domain (0 ≤ η < ∞) are derived by a homotopy analysis method (HAM). Interpretation of various emerging parameters is assigned through graphs for velocity and temperature distributions and tables for surface heat transfer. The present results are compared with the previous studies in limiting cases and results are found in very good agreement. © 2011 Wiley Periodicals, Inc. Heat Trans Asian Res; Published online in Wiley Online Library (wileyonlinelibrary.com/journal/htj). DOI 10.1002/htj.20381
Fibronectin attachment protein from bacillus Calmette‐Guerin as targeting agent for bladder tumor cells
Authors: Coon Brian G. , Crist Scott , González‐Bonet Andrés M. , Kim Hee‐Kwon , Sowa Jennifer , Thompson David H. , Ratliff Timothy L. , Aguilar R. Claudio 
Published: September 2011

AbstractThe adjuvant therapy of choice for superficial bladder cancer is the intravesical instillation of live Mycobacterium bovis bacillus Calmette‐Guerin (BCG). Despite the fact that this therapy is the most effective treatment for superficial bladder cancer, intravesical administration of BCG is associated with high local morbidity and the potential for systemic infection. Therefore, there is a need for the development of safer, less toxic approaches to fight this disease. Because fibronectin attachment protein (FAP) is a key element in BCG retention and targeting to cells, we hypothesize that this protein can be used as targeting agent to deliver cytotoxic cargo for the treatment of bladder tumors. Here, we evaluated the ability of bladder tumor cells to bind and endocytose FAP via fibronectin–integrin complexes. We found that microaggregation induced by an anti‐FAP polyclonal antibody accelerated FAP uptake by T24 bladder tumor cells. FAP was determined to be internalized via a clathrin‐independent, caveolae‐dependent mechanism. Furthermore, once within the endosomal compartment, FAP was targeted to the lysosomal compartment with negligible recycling to the plasma membrane. Importantly, we demonstrated that FAP microaggregation and internalization could also be triggered by multivalent Ni2+NTA‐bearing liposomes. Overall, our studies validate the use of FAP as a targeting vector and provide the foundation for the design of more effective, less‐toxic bladder cancer therapeutics.
Urokinase plasminogen activator receptor on invasive cancer cells: A prognostic factor in distal gastric adenocarcinoma
Authors: Alpízar‐Alpízar Warner , Christensen Ib Jarle , Santoni‐Rugiu Eric , Skarstein Arne , Ovrebo Kjell , Illemann Martin , Laerum Ole Didrik 
Published: September 2011

AbstractGastric cancer is the second cancer causing death worldwide. The five‐year survival for this malignancy is below 25% and few parameters have shown an impact on the prognosis of the disease. The receptor for urokinase plasminogen activator (uPAR) is involved in extracellular matrix degradation by mediating cell surface associated plasminogen activation, and its presence on gastric cancer cells is linked to micrometastasis and poor prognosis. Using immunohistochemistry, the prognostic significance of uPAR was evaluated in tissue samples from a retrospective series of 95 gastric cancer patients. uPAR was expressed by neoplastic cells, macrophages, myofibroblasts and neutrophils in both intestinal and diffuse subtypes. No association was demonstrated between the expression of uPAR on cancer cells and histological subtype (p = 0.64) or TNM stage (p = 0.75). Univariate analysis revealed a significant association between the expression of uPAR on tumor cells in the peripheral invasion zone and overall survival of gastric cancer patients (HR = 2.16; 95% CI: 1.13–4.14; p = 0.02). Multivariate analysis showed that uPAR immunoreactivity in cancer cells at the invasive front is an independent prognostic factor for overall survival in gastric cancer (HR = 2.39; 95% CI: 1.22–4.69; p = 0.011). In consequence, scoring of uPAR‐positive cancer cells may be a direct measure for the invasive potential of gastric adenocarcinomas.
Neural integration of reward, arousal, and feeding: Recruitment of VTA, lateral hypothalamus, and ventral striatal neurons
Authors: Gutierrez Ranier , Lobo Mary Kay , Zhang Feng , de Lecea Luis 
Published: September 2011

AbstractThe ability to control neuronal activity using light pulses and optogenetic tools has revealed new properties of neural circuits and established causal relationships between activation of a single genetically defined population of neurons and complex behaviors. Here, we briefly review the causal effect of activity of six genetically defined neural circuits on behavior, including the dopaminergic neurons DA in the ventral tegmental area (VTA); the two main populations of medium‐sized spiny neurons (D1‐ and D2‐positive) in the striatum; the giant Cholinergic interneurons in the ventral striatum; and the hypocretin‐ and MCH‐ expressing neurons in the lateral hypothalamus. We argue that selective spatiotemporal recruitment and coordinated spiking activity among these cell type‐specific neural circuits may underlie the neural integration of reward, learning, arousal and feeding. © 2011 IUBMB IUBMB Life, 2011
CD38 through the life of a murine B lymphocyte
Authors: Vences‐Catalán Felipe , Santos‐Argumedo Leopoldo 
Published: September 2011

AbstractCD38 is a 45 kDa transmembrane receptor expressed in B lymphocytes and other cells from the immune system. It is involved in apoptosis, cell activation, differentiation, and proliferation. CD38 has been used extensively to classify various subpopulations of lymphocytes in both humans and mice. It has also been used as a marker of poor prognosis in some lymphoid pathologies. However, CD38 is not a marker but rather an ectoenzyme and a receptor, where it performs several functions. The CD38 signaling pathway has only been partially studied in various cells of the immune system, where apparently the signaling is different depending on the lineage and differentiation state of the cell, leading to distinct outcomes. In this review, we provide an overview of well‐established roles of CD38 signaling B lymphocytes from mice. We also discuss areas that need further clarification to get a broader image of how CD38 performs different functions in B cells and to understand its role in B lymphocyte biology under normal versus pathological conditions. © 2011 IUBMB IUBMB Life, 2011
Progesterone and 17β‐estradiol increase differentiation of mouse embryonic stem cells to motor neurons
Authors: López‐González Rodrigo , Camacho‐Arroyo Ignacio , Velasco Iván 
Published: September 2011

AbstractEmbryonic stem (ES) cells have the capacity to differentiate into endodermal, mesodermal, and ectodermal lineages. Motor neuron (MN) differentiation of mouse ES cells involves embryoid bodies formation with addition of Sonic hedgehog and retinoic acid. In this work, using immunocytochemistry, flow cytometry, and quantitative RT‐PCR, we investigated whether progesterone or 17β‐estradiol have inductive effects on ES cell‐derived MN, as it has been demonstrated that these hormones modify proliferation and neural differentiation of pluripotent cells. When 100 nM progesterone was added during differentiation, we found higher proportions of MN, compared to the control condition; coincubation of progesterone with the progesterone receptor (PR) antagonist RU‐486 caused a decrease in the number of MN to a percentage even lower than controls. The addition of nanomolar concentrations of 17β‐estradiol also significantly induced MN differentiation. This effect of estradiol was completely antagonized by addition of the general estrogen receptor (ER) antagonist ICI 182,780. To identify the ER subtype mediating the increase on MN differentiation, we incubated estradiol with the ER‐α antagonist MPP or with the ER‐β blocker PHTPP. When we coincubated 17β‐estradiol with MPP, we found a significant decrease in the percentage of MN. In contrast, the coincubation of 17β‐estradiol with PHTPP had no effect on the induction of MN differentiation. All these effects on cell number were confirmed by significant changes in the expression of the MN markers Islet‐1 and Choline acetyl transferase, assessed by real‐time RT‐PCR. Cell proliferation in embryoid bodies was significantly enhanced by progesterone treatment. No changes in apoptotic cell death were found in differentiating cells after progesterone or 17β‐estradiol addition. Our findings indicate that progesterone and 17β‐estradiol induce a higher proportion of MN derived from mouse ES cells through intracellular PR and ER, respectively. Furthermore, the effect of estradiol was mediated by specific activation of ER‐α. © 2011 IUBMB IUBMB Life, 2011