bluuebunny/crossref_metadata_2025_split huggingface dataset:
Topographic controls on shallow groundwater dynamics: implications of hydrologic connectivity between hillslopes and riparian zones in a till mantled catchment
Authors: Detty J. M. , McGuire K. J. 
Published: March 2010

AbstractHydrologic connectivity is regarded as one of the key controls in determining catchment rainfall–run‐off response and has been linked to the export of solutes from uplands to streams. We sought to identify the patterns of hydrologic connectivity within a small forested watershed by monitoring the shallow groundwater fluctuations of simple topographically defined landform sequences (footslope–backslope–shoulder). A spatially distributed instrument network was employed to continuously measure hydrometric responses of the shallow subsurface during seasonal wet‐up from summer through winter in a small till mantled research catchment. We demonstrate that the spatial patterns of shallow water table extent and duration, and therefore hydrologic connectivity, had a strong seasonal signature. During the low antecedent soil moisture conditions typically associated with the growing season, water tables were patchy, discontinuous, and only the wettest near‐stream footslope areas were consistently hydrologically connected with the stream network. During the dormant season, footslopes and backslopes maintained water tables that persisted between storm events and were almost continuously connected with the stream network. In the largest storm events, the typically driest landforms (shoulder slopes) established shallow transient water tables, suggesting that nearly the entire catchment was temporarily hydrologically connected with the stream network. In addition, we found significant differences (p < 0·05) in the magnitude and duration of groundwater responses to rainfall among landform groups both seasonally and during events. These results have implications for using a similarity approach in representing characteristic hydrologic responses of topographically defined watershed elements, determining hydrologic connectivity between watershed elements, as well as for understanding solute transport in catchments. Copyright © 2010 John Wiley & Sons, Ltd.
Polymer LEDs as a physics tool
Authors: Tessler Nir , Cleave Vicki , Pinner Dickon J. 
Published: March 2010

AbstractWe present a systematic experimental and theoretical study of physical mechanisms governing the operation of polymer light‐emitting diodes. We show that through self‐consistent modeling we can address both charge transport and exciton generation. Electron and hole mobility in several polymers has been characterized experimentally. Characterization of excitons and especially of triplet‐excitons is achieved through use of a triplet‐emitting molecule.
Polymorphonuclear leukocyte inhibition of monocytes/macrophages in the foreign body reaction
Authors: Kirk James T. , McNally Amy K. , Anderson James M. 
Published: March 2010

AbstractThe effect of polymorphonuclear leukocytes (PMNs) on the subsequent chronic phase macrophage‐mediated foreign body reaction has not been previously investigated. Furthermore, while monocyte/macrophage‐produced cytokines such as GM‐CSF, G‐CSF, or IL‐1β have been shown to increase PMN survival in vitro, few studies have examined the impact of directly cocultured monocytes/macrophages on PMN viability. To this end, we used our established in vitro system of interleukin (IL)‐4‐induced monocyte‐derived macrophage fusion to examine the role of PMNs in the subsequent foreign body reaction. Monocytes were directly cultured with PMNs for 3 days before the addition of IL‐4 to induce monocyte‐derived macrophage fusion to facilitate foreign body giant cell (FBGC) formation by days 7 and 10 of culture. Optical microscopy was used to quantitatively determine adherent monocyte density, percent macrophage fusion, and FBGC density. A colorimetric MTT assay was used to assess PMN viability for direct cocultures of monocytes/macrophages and PMNs. Our results strongly suggest that the presence of PMNs inhibit IL‐4‐induced macrophage fusion and FBGC formation. Additionally, our findings demonstrate that cocultures containing PMNs and monocytes/macrophages increases PMN survival with respect to PMN‐only cultures in vitro. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010
Low molecular weight hyaluronic acid effects on murine macrophage nitric oxide production
Authors: Lyle Daniel B. , Breger Joyce C. , Baeva Larissa F. , Shallcross Jonathan C. , Durfor Charles N. , Wang Nam Sun , Langone John J. 
Published: March 2010

AbstractHyaluronic acid (HA) is increasingly used for a number of medical device applications. Since the chemical structure of HA is identical no matter its bacterial or animal origin, it should be the ideal biomaterial. However, short term transient inflammatory reactions are common, while rare long‐term adverse events may correlate with subclinical chronic inflammation. Concern has been raised that low molecular weight components or degradation fragments from implanted HA may directly stimulate inflammatory reactions. This study examined a panel of HA molecular weights from the unitary disaccharide up to 1.7 × 106 Dalton lengths, in which endotoxin was assayed at a very low level (less than 0.03 EU/mg). The murine cell line RAW 264.7, rat splenocytes, and rat adherent differentiated primary macrophages were assayed for nitric oxide production under a variety of inflammatory conditions plus or minus HA. Under the highest inflammatory states, nitric oxide production was mildly suppressed by HMW‐HA while slightly augmented by LMW‐HA at mg/mL concentrations. However, at micromolar concentrations fragments below 5000 Daltons, thought to have drug‐like qualities, were without effect. These data support the hypothesis that if endotoxin is reduced to an extremely low level, LMW‐HA may not directly provoke normal tissue macrophage‐mediated inflammatory reactions. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010
Effect of bone graft substitute on marrow stromal cell proliferation and differentiation
Authors: Siggers Kevin , Frei Hanspeter , Fernlund Göran , Rossi Fabio 
Published: March 2010

AbstractMarrow stromal cells (MSCs) are ideally suited for tissue engineered bone grafts since they have the potential to regenerate bone, but may also maintain the homeostasis of the repaired tissue through their ability for self‐renewal. An ideal bone graft substitute should support MSC self‐renewal as well as differentiation to ensure complete bone defect regeneration and maintenance. The purpose of this investigation was to determine the effect of different substrate materials on MSC expansion and differentiation. Calcium polyphosphate (CPP), bone and hydroxyapatite/tricalcium phosphate (HA/TCP) were seeded with rat MSCs and maintained in culture conditions that promote cell expansion. At 0, 3, 7, 14, and 21 days cell numbers were determined by measuring their metabolic activity using a MTT assay and the frequency of cycling cells by 24 hr BrdU incorporation. Osteogenic, chondrogenic, and adipogenic marker expression in these cultures was measured by qRT‐PCR. An initial drop in cell numbers was observed on all substrates. CPP and bone, but not HA/TCP supported an increase in proliferating cells at day 14 and 21. In addition, no upregulation of mature bone markers was observed in cells cultured on CPP and bone, which suggests that these substrates support the expansion of undifferentiated MSCs. In contrast, cell numbers on HA/TCP decreased with time and only rare BrdU positive cells were observed. This decrease in proliferation correlated with the down regulation of osteogenic progenitor markers and the substantial increase in mature osteocyte markers, indicating that HA/TCP favors MSC differentiation and maturation along the osteogenic lineage. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A, 2010
Articular cartilage tissue engineering based on a mechano‐active scaffold made of poly(L‐lactide‐co‐ε‐caprolactone): In vivo performance in adult rabbits
Authors: Xie Jun , Han Zhiyi , Naito Masatoshi , Maeyama Akira , Kim Soo Hyun , Kim Young Ha , Matsuda Takehisa 
Published: March 2010

AbstractOur previous studies showed that a mechano‐active scaffold made of poly(L‐lactide‐co‐ε‐caprolactone) (PLCL) exhibited a high potential to realize the formation of a functional, engineered cartilage in vitro. This animal study therefore was designed to investigate the feasibility of repairing on osteochondral defect with the use of bone marrow‐derived mesenchymal stem cells (BMSCs) incorporated with a PLCL scaffold. Rabbit BMSCs, isolated and subsequently cultured in monolayer, were seeded into a porous PLCL scaffold sponge following an implantation onto a full‐thickness osteochondral defect (diameter of 4.5 mm, depth of 5 mm) that was artificially created on the medial femoral condyles at a high load‐bearing site on a rabbit's knee joint. Time‐dependent healing of the defect was evaluated by macroscopic, histological examinations at both 3‐ and 6‐month‐implantations, respectively. A PLCL sponge incorporated with BMSCs exhibited sufficient structural support, resulting in new osteochondral tissue regeneration: a physiologically well‐integrated subchondral bone formation, a hyaline cartilage‐like morphology containing chondrocytes surrounded by abundant cartilaginous matrices. In addition, quantitative biochemical assays also demonstrated high potential for the synthesis of sulfated glycosaminoglycan and collagen, both of which are biomolecules essential to extracelluar matrix in normal cartilage tissue. In contrast, defects filled with cell‐free PLCL scaffold or left empty showed a very limited potential for regeneration. Our findings suggest that a composite of PLCL‐based sponge scaffold and BMSCs promote the repair of osteochondral defects at high load‐bearing sites in adult rabbits. © 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2010
High-phosphate-induced calcification is related to SM22α promoter methylation in vascular smooth muscle cells
Authors: de Oca Addy Montes , Madueño Juan A , Martinez-Moreno Julio M , Guerrero Fatima , Muñoz-Castañeda Juan , Rodriguez-Ortiz Marien E , Mendoza Francisco J , Almaden Yolanda , Lopez Ignacio , Rodriguez Mariano , Aguilera-Tejero Escolastico 
Published: March 2010

Abstract
Hyperphosphatemia is closely related to vascular calcification in patients with chronic kidney disease. Vascular smooth muscle cells (VSMCs) exposed to high phosphate concentrations in vitro undergo phenotypic transition to osteoblast-like cells. Mechanisms underlying this transdifferentiation are not clear. In this study we used two in vitro models, human aortic smooth muscle cells and rat aortic rings, to investigate the phenotypic transition of VSMCs induced by high phosphate. We found that high phosphate concentration (3.3 mmol/L) in the medium was associated with increased DNA methyltransferase activity and methylation of the promoter region of SM22α. This was accompanied by loss of the smooth muscle cell–specific protein SM22α, gain of the osteoblast transcription factor Cbfa1, and increased alkaline phosphatase activity with the subsequent in vitro calcification. The addition of a demethylating agent (procaine) to the high-phosphate medium reduced DNA methyltransferase activity and prevented methylation of the SM22α promoter, which was accompanied by an increase in SM22α expression and less calcification. Additionally, downregulation of SM22α, either by siRNA or by a methyl group donor (S-adenosyl methionine), resulted in overexpression of Cbfa1. In conclusion, we demonstrate that methylation of SM22α promoter is an important event in vascular smooth muscle cell calcification and that high phosphate induces this epigenetic modification. These findings uncover a new insight into mechanisms by which high phosphate concentration promotes vascular calcification. © 2010 American Society for Bone and Mineral Research
Mechanism underlying long‐term regulation of 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase during L6 myoblast differentiation
Authors: Trapani Laura , Martini Chiara , Trentalance Anna , Pallottini Valentina 
Published: March 2010

Abstract3‐Hydroxy 3‐methylglutaryl Coenzyme A reductase (HMG‐CoAR) and its end‐products are crucial for insulin‐induced differentiation of fetal rat myoblasts (L6) both at early and terminal stages of development. Inhibition of HMG‐CoAR activity and reduction of the enzyme levels impair the expression of L6 differentiation markers and prevent myoblast fusion into multinucleated syncytia. The mechanism underlying the modulation of this crucial enzyme so that muscular differentiation can occur is poorly understood. Thus, the aim of this work was to explore the long‐term regulation of HMG‐CoAR in an attempt to provide a new molecular basis for the control of muscle development. All experiments were performed in L6 rat myoblasts induced to differentiate utilizing insulin. The results indicate the following: (i) at early stages of L6 differentiation, the increase in HMG‐CoAR protein levels is probably due to transcriptional induction and a decrease in the enzyme degradation rate; (ii) the subsequent reduction of HMG‐CoAR protein levels is related both to an increased degradation rate and reduced gene transcription, as indicated by the rise of Insig‐1 levels and the subsequent decrease in the amount of n‐SREBP‐1; (iii) in the terminal stages of myogenesis, reduced protein levels of HMG‐CoAR could be ascribed to the decrease in gene transcription while its degradation rate is not affected. By highlighting the mechanisms involved in HMG‐CoAR long‐term regulation during myogenesis, this work provides useful information for searching for tools to improve the regenerative ability of muscle tissue and for the development of new pharmacological treatments of myopathies. J. Cell. Biochem. 110: 392–398, 2010. © 2010 Wiley‐Liss, Inc.
TRAIL/TRAIL‐R in hematologic malignancies
Authors: Testa Ugo 
Published: March 2010

AbstractDefects in apoptosis are observed in many cancer cell types and contribute in a relevant way to tumorigenesis. Apoptosis is a complex and well‐regulated cell death program that plays a key role in the control of cell homeostasis, particularly at the level of the hematopoietic system. Apoptosis can be initiated through two different mechanisms involving either activation of the death receptors (extrinsic pathway) or activation of a mitochondrial apoptotic process (intrinsic pathway). Among the various death receptors a peculiar role is played by TNF‐related apoptosis‐inducing ligand (TRAIL)‐receptors (TRAIL‐Rs) and their ligand TRAIL. TRAIL recently received considerable interest for its potent anti‐tumor killing activity, sparing normal cells. Here, we will review the expression and the abnormalities of TRAIL/TRAIL‐R system in hematologic malignancies. The large majority of primary hematologic tumors are resistant to TRAIL‐mediated apoptosis, basically due to the activation of anti‐apoptotic signaling pathway (such as NF‐κB), overexpression of anti‐apoptotic proteins (such as FLIP, Bcl‐2, XIAP) or expression of TRAIL decoy receptors or reduced TRAIL‐R1/‐R2 expression. Strategies have been developed to bypass this TRAIL resistance and are based on the combination of TRAIL with chemotherapy or radiotherapy, or with proteasome or histone deacetylase or NF‐κB inhibitors. The agents used in combination with TRAIL either enhance TRAIL‐R1/‐R2 expression or decrease expression of anti‐apoptotic proteins (c‐FLIP, XIAP, Bcl‐2). Many of these combinatorial therapies hold promise for future developments in treatment of hematologic malignancies. J. Cell. Biochem. 110: 21–34, 2010. © 2010 Wiley‐Liss, Inc.
Piscirickettsia salmonis induces apoptosis in macrophages and monocyte‐like cells from rainbow trout
Authors: Rojas Verónica , Galanti Norbel , Bols Niels C. , Jiménez Verónica , Paredes Rodolfo , Marshall Sergio H. 
Published: March 2010

AbstractPiscirickettsia salmonis is the etiologic agent of the salmonid rickettsial septicemia (SRS) which causes significant losses in salmon production in Chile and other and in other regions in the southern hemisphere. As the killing of phagocytes is an important pathogenic mechanism for other bacteria to establish infections in vertebrates, we investigated whether P. salmonis kills trout macrophages by apoptosis. Apoptosis in infected macrophages was demonstrated by techniques based on morphological changes and host cell DNA fragmentation. Transmission electron microcopy showed classic apoptotic characteristics and terminal deoxynucleotidyl transferase‐mediated dUTP nick end labeling showed fragmented DNA. Programmed cell death type I was further confirmed by increased binding of annexin V to externalized phosphatidylserine in infected macrophages. Moreover, significant increases of caspase 3 activation were detected in infected cells and treatment with caspase inhibitor caused a decrease in levels of apoptosis. This is the first evidence that P. salmonis induces cell death in trout macrophages. This could lead to bacterial survival and evasion of the host immune response and play an important role in the establishment of infection in the host. J. Cell. Biochem. 110: 468–476, 2010. © 2010 Wiley‐Liss, Inc.
Pentapeptide insertion mutagenesis of the Hoxa1 protein: Mapping of transcription activation and DNA‐binding regulatory domains
Authors: Lambert Barbara , Vandeputte Julie , Desmet Pierre‐Marie , Hallet Bernard , Remacle Sophie , Rezsohazy René 
Published: March 2010

AbstractThe mode of action of Hoxa1, like that of most Hox proteins, remains poorly characterized. In an effort to identify functional determinants contributing to the activity of Hoxa1 as a transcription factor, we generated 18 pentapeptide insertion mutants of the Hoxa1 protein and we assayed them in transfected cells for their activity on target enhancers from the EphA2 and Hoxb1 genes known to respond to Hoxa1 in the developing hindbrain. Only four mutants displayed a complete loss‐of‐function. Three of them contained an insertion in the homeodomain of Hoxa1, whereas the fourth loss‐of‐function mutant harbored an insertion in the very N‐terminal end of the protein. Transcription activation assays in yeast further revealed that the integrity of both the N‐terminal end and homeodomain is required for Hoxa1‐mediated transcriptional activation. Furthermore, an insertion in the serine–threonine–proline rich C‐terminal extremity of Hoxa1 induced an increase in activity in mammalian cells as well as in the yeast assay. The C‐terminal extremity thus modulates the transcriptional activation capacity of the protein. Finally, electrophoretic mobility shift assays revealed that the N‐terminal extremity of the protein also exerts a modulatory influence on DNA binding by Hoxa1–Pbx1a heterodimers. J. Cell. Biochem. 110: 484–496, 2010. © 2010 Wiley‐Liss, Inc.
Calcium oscillations induced by gambierol in cerebellar granule cells
Authors: Alonso E. , Vale C. , Sasaki M. , Fuwa H. , Konno Y. , Perez S. , Vieytes M.R. , Botana L.M. 
Published: March 2010

AbstractGambierol is a marine polyether ladder toxin derived from the dinoflagellate Gambierdiscus toxicus. To date, gambierol has been reported to act either as a partial agonist or as an antagonist of sodium channels or as a blocker of voltage‐dependent potassium channels. In this work, we examined the cellular effect of gambierol on cytosolic calcium concentration, membrane potential and sodium and potassium membrane currents in primary cultures of cerebellar granule cells. We found that at concentrations ranging from 0.1 to 30 µM, gambierol‐evoked [Ca2+]c oscillations that were dependent on the presence of extracellular calcium, irreversible and highly synchronous. Gambierol‐evoked [Ca2+]c oscillations were completely eliminated by the NMDA receptor antagonist APV and by riluzole and delayed by CNQX. In addition, the K+ channel blocker 4‐aminopyridine (4‐AP)‐evoked cytosolic calcium oscillations in this neuronal system that were blocked by APV and delayed in the presence of CNQX. Electrophysiological recordings indicated that gambierol caused membrane potential oscillations, decreased inward sodium current amplitude and decreased also outward IA and IK current amplitude. The results presented here point to a common mechanism of action for gambierol and 4‐AP and indicate that gambierol‐induced oscillations in cerebellar neurons are most likely secondary to a blocking action of the toxin on voltage‐dependent potassium channels and hyperpolarization of sodium current activation. J. Cell. Biochem. 110: 497–508, 2010. © 2010 Wiley‐Liss, Inc.
Investigation of binding features: Effects on the interaction between CYP2A6 and inhibitors
Authors: Ai Chunzhi , Li Yan , Wang Yonghua , Li Wei , Dong Peipei , Ge Guangbo , Yang Ling 
Published: March 2010

AbstractA computational investigation has been carried out on CYP2A6 and its naphthalene inhibitors to explore the crucial molecular features contributing to binding specificity. The molecular bioactive orientations were obtained by docking (FlexX) these compounds into the active site of the enzyme. And the density functional theory method was further used to optimize the molecular structures with the subsequent analysis of molecular lipophilic potential (MLP) and molecular electrostatic potential (MEP). The minimal MLPs, minimal MEPs, and the band gap energies (the energy difference between the highest occupied molecular orbital and lowest unoccupied molecular orbital) showed high correlations with the inhibition activities (pIC50s), illustrating their significant roles in driving the inhibitor to adopt an appropriate bioactive conformation oriented in the active site of CYP2A6 enzyme. The differences in MLPs, MEPs, and the orbital energies have been identified as key features in determining the binding specificity of this series of compounds to CYP2A6 and the consequent inhibitory effects. In addition, the combinational use of the docking, MLP and MEP analysis is also demonstrated as a good attempt to gain an insight into the interaction between CYP2A6 and its inhibitors. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
A computational study on the capability of borane‐cyclic boryl anion adducts to act as hydrogen atom donors
Authors: Lai Chin‐Hung , Chou Pi‐Tai 
Published: March 2010

AbstractAccording to our theoretical approaches, a cyclic boryl anion can act as a Lewis base like its isoelectronic counterpart N‐heterocyclic carbene, reducing the homolytic bond dissociation energy of BH in BH3. However, the donating efficiency is affected by the counter cation in both gas phase and nonpolar solvents. Moreover, we also predict the seven‐membered ring boryl anion 5, although it has not yet synthesized, to be the most efficient reagent to reduce the bond dissociation energy of a BH bond in BH3. This study may thus pave another avenue toward Lewis base induced hydrogen atom abstraction in BH3. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010