bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cellular cholesterol efflux to serum is impaired in diabetic nephropathy
Authors: Zhou Huali , Tan Kathryn C. B. , Shiu Sammy W. M. , Wong Ying 
Published: September 2008

AbstractBackgroundCholesterol efflux from cells is an early step of reverse cholesterol transport (RCT) and the capacity of serum to induce cellular cholesterol efflux has recently been shown to be an independent predictor of coronary artery atherosclerosis. Our aim is to evaluate the capacity of serum to induce ATP‐binding cassette transporter A1 (ABCA1) and scavenger receptor class B type I (SR‐BI) mediated cholesterol efflux in type 2 diabetic patients with nephropathy.MethodsDiabetic patients were recruited according to their urinary albumin excretion rate (normoalbuminuria, microalbuminuria and proteinuria) with 20 subjects in each group and compared with 20 age‐matched controls. The ability of the serum to induce cholesterol efflux was measured using a cell culture system.ResultsSerum capacity to induce ABCA1‐mediated cholesterol efflux was decreased in patients with microalbuminuria or proteinuria (p < 0.05) whereas SR‐BI‐mediated cholesterol efflux was impaired in all three groups of diabetic patients (p < 0.05). Plasma high‐density lipoprotein (HDL) cholesterol and apoAI were reduced in all groups of diabetic patients, but pre‐β‐HDL was only significantly decreased in those with microalbuminuria or proteinuria. Serum advanced glycation end products (AGEs) were significantly increased in diabetic patients with microalbuminuria or proteinuria. Serum AGEs and pre‐β‐HDL were the significant independent determinants of ABCA1‐mediated cholesterol efflux, whereas plasma HDL and log (creatinine) were the significant determinants of SR‐BI‐mediated cholesterol efflux.ConclusionThe capacity of serum to induce ABCA1‐ and SR‐BI‐mediated cholesterol efflux was impaired in diabetic patients with incipient or overt nephropathy. These abnormalities may contribute to the accelerated development of atherosclerotic vascular disease in these patients. Copyright © 2008 John Wiley & Sons, Ltd.
Conservation of notochord gene expression across chordates: Insights from the Leprecan gene family
Authors: Capellini Terence D. , Dunn Matthew P. , Passamaneck Yale J. , Selleri Licia , Di Gregorio Anna 
Published: September 2008

AbstractThe notochord is a defining character of the chordates, and the T‐box transcription factor Brachyury has been shown to be required for notochord development in all chordates examined. In the ascidian Ciona intestinalis, at least 44 notochord genes have been identified as bona fide transcriptional targets of Brachyury. We examined the embryonic expression of a subset of murine orthologs of Ciona Brachyury target genes in the notochord to assess its conservation throughout chordate evolution. We focused on analyzing the Leprecan gene family, which in mouse is composed of three genes, as opposed to the single‐copy Ciona gene. We found that all three mouse Leprecan genes are expressed in the notochord. Additionally, while Leprecan expression in C. intestinalis is confined to the notochord, expression of its mouse orthologs includes dorsal root ganglia, limb buds, branchial arches, and developing kidneys. These results have interesting implications for the evolution and development of chordates. genesis 46:683–696, 2008. © 2008 Wiley‐Liss, Inc.
Phenotypic analyses of a medaka mutant reveal the importance of bilaterally synchronized expression of isthmic fgf8 for bilaterally symmetric formation of the optic tectum
Authors: Takashima Shigeo , Kage Takahiro , Yasuda Takako , Inohaya Keiji , Maruyama Kouichi , Araki Kazuo , Takeda Hiroyuki , Ishikawa Yuji 
Published: September 2008

AbstractDeveloping neural tubes are bilaterally symmetric in all vertebrate embryos, irrespective of the presence of gene networks that generate left‐right asymmetry. To explore the mechanisms that underlie the bilaterally symmetric formation of the neural tube, we examined a medaka (Oryzias latipes) dominant mutant, Oot, the neural tube of which transiently lacks normal symmetry in the optic tectum. We found that spatial changes in isthmic fgf8 expression do not occur on one side of the mutant, resulting in a transient desynchronized expression that correlates with tectal asymmetry. The application of exogenous FGF8 on one side of a wild‐type embryo mimics the Oot phenotype, indicating that the bilaterally equivalent expression of isthmic fgf8 is crucial for the bilaterally symmetric development of the tectum. These results suggest that tectal symmetry is not a “default” state, but rather is maintained actively by a bilaterally coupled and synchronized regulation of isthmic fgf8 expression. genesis 46:537–545, 2008. © 2008 Wiley‐Liss, Inc.
Generation of a conditional null allele for Cftr in mice
Authors: Hodges Craig A. , Cotton Calvin U. , Palmert Mark R. , Drumm Mitchell L. 
Published: September 2008

AbstractThe cystic fibrosis transmembrane conductance regulator (CFTR) gene encodes a cAMP‐regulated chloride channel that is important in controlling the exchange of fluid and electrolytes across epithelial cells. Mutation of CFTR can lead to cystic fibrosis (CF), the most common lethal genetic disease in Caucasians. CF is a systemic illness with multiple organ systems affected including pulmonary, gastrointestinal, pancreatic, immune, endocrine, and reproductive systems. To understand the role of CFTR in the various tissues in which it is expressed, we generated a murine conditional null allele of Cftr (Cftrfl10) in which loxP sites were inserted around exon 10 of the Cftr gene. The Cftrfl10 allele was validated by generating constitutive Cftr null (CftrΔ10) mice using the protamine‐cre system. The CftrΔ10/Δ10 mice displayed almost identical phenotypes to previously published CF mouse models, including poor growth, decreased survival, intestinal obstruction, and loss of Cftr function as assessed by electrophysiology measurements on gut and nasal epithelium. Mice containing the conditional null Cftr allele will be useful in future studies to understand the role of Cftr in specific tissues and developmental time points and lead to a better understanding of CF disease. genesis 46:546–552, 2008. © 2008 Wiley‐Liss, Inc.
Stem‐Loop DNA Probes for the Voltammetric Determination of Legionella pneumophila on Disposable Screen‐Printed Gold Electrodes
Authors: Miranda‐Castro Rebeca , Lobo‐Castañón M. Jesús , Miranda‐Ordieres Arturo J. , Tuñón‐Blanco Paulino 
Published: September 2008

AbstractA disposable voltammetric sensor for the detection of DNA sequences specific of Legionella pneumophila is presented. The sensor is based on a sandwich‐hybridization format assay, using a stem‐loop DNA structure as capture probe immobilized onto a screen‐printed gold electrode. The signaling‐DNA probe is labeled with biotin, and streptavidin‐alkaline phosphatase is used as reporter molecule. 1‐Naphthol, the enzymatic hydrolysis product of α‐naphthyl phosphate, is voltammetrically detected. The hairpin‐modified screen‐printed gold electrode allows the detection of a 52‐mer DNA sequence at 400 pM level. With a sample volume of 40 μL, this concentration corresponds to ca. 16 fmol of a DNA sequence specific of L. pneumophila. The analytical performance of this platform is compared with that previously obtained for a sensor constructed on a conventional disk gold electrode with the same geometry (Ø=1.6 mm) and design. A lower quantification limit is obtained with the SPE. In addition, the selectivity is improved as the disposable device shows a better discrimination between L. pneumophila and L. longbeachae or L. micdadei under identical nonstringent conditions.
Synthesis and Characterization of Novel Nanophase Hexagonal Poly(2,5‐dimethoxyaniline)
Authors: Mavundla Sipho E. , Malgas Gerald F. , Baker Priscilla , Iwuoha Emmanuel. I. 
Published: September 2008

AbstractNovel nanophase hexagonal structured polyaniline (PANI) and poly(2,5‐dimethoxyanilines) (PDMA) were synthesized by oxidative polymerization involving the respective anilines and a mixture of ferric chloride and ammonium persulfate. The morphological, spectral and electrochemical characteristics of the polymers were determined from the results of SEM, FTIR, UV‐vis, TGA and cyclic voltammetry experiments. The hexagonal PANI and PDMA nanorods (15–200 nm diameter) exhibited very good thermal stabilities, losing only 10% of their weight on heating to 400 °C. Electrochemical data indicated a pernigraniline state of the polymers with formal potential, E°′, values of 394±6 mV and 400±1 mV, for PANI (conductance, C=0.37×10−3 S) and PDMA (conductance, C=2.02×10−3 S), respectively. The pernigraniline state was confirmed by sharp FTIR pernigraniline quinoidic peaks (PANI: 1414 cm−1; PDMA: 1157 cm−1), and UV‐vis absorption maxima at 340–370 nm (PANI) and 450–650 nm (PDMA) which are characteristic of charge transfer excitons of the quinoid structures of pernigraniline.
CuO Nanospheres Based Nonenzymatic Glucose Sensor
Authors: Reitz Eliot , Jia Wenzhao , Gentile Michael , Wang Ying , Lei Yu 
Published: September 2008

AbstractCuO nanospheres, synthesized by a simple one‐step hydrothermal method, have been applied to modify the glassy carbon (GC) electrode for sensitive nonenzymatic glucose detection. The CuO nanospheres modified electrode, compared to the Nafion modified GC electrode, exhibits an enhanced electrocatalytic property for direct glucose oxidation and shows a fast response and a high sensitivity for the amperometric detection of glucose. It has been determined that the dissolved oxygen is not involved in glucose oxidation and the high concentration of NaCl does not poison the electrode. These results also indicate that CuO nanospheres have great potential application in electrochemical detection.
Self‐centering steel connections with steel bars and a discontinuous composite slab
Authors: Chou Chung‐Che , Tsai Keh‐Chyuan , Yang Wen‐Chia 
Published: September 2008

AbstractSix cyclic tests were conducted on three full‐scale subassemblies to investigate the behavior of interior beam‐to‐column post‐tensioned (PT) connections. Strands were placed along each side of the steel beam web, passing through the steel column to provide precompression between the beams and a column. Top and bottom energy‐dissipating (ED) bars, passing through the column and welded to the beam, were used to increase the moment capacity and ED capacity of the connection. One of the subassemblies also had a composite concrete slab with discontinuity at the column centerline to eliminate restraint from the metal deck, reinforcement, and welded wire mesh. The objectives of this paper were to investigate the following: the durability of the connection by loading each specimen twice, the ED capacity of the ED bar, and the effects that the type of ED bar and type of composite slab have on the self‐centering behavior of the connection. The experimental results showed that: (1) the connection could sustain severe inelastic cyclic loading at least twice without strength degradation, (2) the ED capacity of the bar was much larger than that dissipated by a single AISC loading protocol, and (3) a specimen with a discontinuous composite slab, which opened freely at the centerline of the column, ensured the same self‐centering hysteretic behavior as the bare steel specimen. However, the decompression moment of the PT connection decreased significantly at each interstory drift, resulting in an early opening of a gap at the beam–column interface. Copyright © 2008 John Wiley & Sons, Ltd.
Leptin regulation of proangiogenic molecules in benign and cancerous endometrial cells
Authors: Carino Cecilia , Olawaiye Alexander B. , Cherfils Salandre , Serikawa Takehiro , Lynch Maureen P. , Rueda Bo R. , Gonzalez Ruben R. 
Published: September 2008

AbstractSeveral proangiogenic/proinflammatory factors involved in endometrial cancer are regulated by leptin, but the signaling mechanisms responsible for these leptin‐induced actions are largely unknown. Here, we report that in benign (primary and HES) and cancerous‐endometrial epithelial cells (EEC) (An3Ca, SK‐UT2 and Ishikawa), leptin in a dose‐dependent manner regulates vascular endothelial growth factor, (VEGF); interleukin‐1 beta, (IL‐1β); leukemia inhibitory factor, (LIF) and their respective receptors, VEGFR2, IL‐1R tI and LIFR. Remarkably, leptin induces a greater increase in VEGF/VEGFR2 and LIF levels in cancer than in benign cells. However, IL‐1β was only increased by leptin in benign primary‐EEC. Cancer‐EEC expressed higher levels of leptin receptor (full‐length OB‐Rb and short isoforms) in contrast to benign primary‐EEC. Leptin‐mediated activation of JAK2 (janus kinase 2) was upstream to the activation of PI‐3K (phosphatidylinositol‐3 kinase) and/or MAPK (mitogen‐activated protein kinase) signaling pathways. Leptin induction of cytokines/receptors generally involved JAK2 and MAPK activation, but PI‐3K phosphorylation was required for leptin increase of LIF, IL‐1/IL‐1R tI. Leptin‐mediated activation of mTOR (mammalian target of Rapamycin), mainly linked to MAPK, played a central role in leptin regulation of all cytokines and receptors. These results suggest that leptin's effects are cell‐specific and could confer a proliferative or cell survival advantage or possibly promote endometrial thickness. Leptin's effects on proangiogenic molecules were more evident in malignant versus benign cells and may imply that there is an underlying shift in leptin‐induced cell signaling pathways in endometrial cancer cells. © 2008 Wiley‐Liss, Inc.
Decorin and its galactosaminoglycan chain: Extracellular regulator of cellular function?
Authors: Seidler Daniela G. , Dreier Rita 
Published: September 2008

AbstractA molecular network of extracellular matrix molecules determines the tissue architecture and accounts for mechanical properties like compressibility or stretch resistance. It is widely accepted that the elements of the cellular microenvironment are important regulators of the cellular behavior in vitro and in vivo. One large group comprising these molecules is the family of proteoglycans. Both, the core proteins and, in particular, the attached galactosaminoglycans, contribute to the regulation network as they bind a variety of signaling molecules, e.g. cytokines, chemokines, growth, and differentiation factors. We would like to emphasize specific patterns of epimerization and sulfation within the galactosaminoglycans chains, because these result in “motifs” that are responsible for the modulation of signal factor binding, release and activity. This property is crucial in physiological and pathological conditions, for example development and wound healing. © 2008 IUBMB IUBMB Life, 60(11): 729–733, 2008
How an obscure archaeal gene inspired the discovery of selenocysteine biosynthesis in humans
Authors: Su Dan , Hohn Michael J. , Palioura Sotiria , Sherrer R. Lynn , Yuan Jing , Söll Dieter , O'Donoghue Patrick 
Published: September 2008

AbstractSelenocysteine (Sec) is the 21st genetically encoded amino acid found in organisms from all three domains of life. Sec biosynthesis is unique in that it always proceeds from an aminoacyl‐tRNA precursor. Even though Sec biosynthesis in bacteria was established almost two decades ago, only recently the pathway was elucidated in archaea and eukaryotes. While other aspects of Sec biology have been reviewed previously (Allmang and Krol, Biochimie 2006;88:1561–1571, Hatfield et al., Prog Nucleic Acid Res Mol Biol 2006;81:97–142, Squires and Berry, IUBMB Life 2008;60:232–235), here we review the biochemistry and evolution of Sec biosynthesis and coding and show how the knowledge of an archaeal cysteine biosynthesis pathway helped to uncover the route to Sec formation in archaea and eukaryotes. © 2008 IUBMB IUBMB Life, 61(1): 35–39, 2009
Human head and neck squamous cell carcinoma cells are both targets and effectors for the angiogenic cytokine, VEGF
Authors: Tong Meng , Lloyd Brandon , Pei Ping , Mallery Susan R. 
Published: September 2008

AbstractFormer vascular endothelial growth factor (VEGF)–head and neck squamous cell carcinoma (HNSCC) studies have focused on VEGF's contributions toward tumor‐associated angiogenesis. Previously, we have shown that HNSCC cells produce high levels of VEGF. We therefore hypothesized that VEGF serves a biphasic role, that is, pro‐angiogenic and pro‐tumorigenic in HNSCC pathogenesis. Western blots confirmed the presence of VEGF's primary mitogenic receptors, VEGFR‐2/KDR and VEGFR‐1/Flt‐1 in cultured HNSCC cells. Subsequent studies evaluated VEGF's effects on HNSCC intracellular signaling, mitogenesis, invasive capacities, and matrix metalloproteinases (MMPs) activities. Introduction of hrVEGF165 initiated ROS‐mediated intracellular signaling, resulting in kinase activation and phosphorylation of KDR and Erk1/2. As high endogenous VEGF production rendered HNSCC cells refractory to exogenous VEGF's mitogenic effects, siRNA was employed, inhibiting endogenous VEGF production for up to 96 h. Relative to transfection vector matched controls, siRNA treated HNSCC cells showed a significant decrease in proliferation at both 30 and 50 nM siRNA doses. Addition of exogenous hrVEGF165 (30 and 50 ng/ml) to siRNA‐silenced HNSCC cells resulted in dose‐dependent increases in cell proliferation. Cell invasion assays showed VEGF is a potent HNSCC chemoattractant and demonstrated that VEGF pre‐treatment enhanced invasiveness of HNSCC cells. Conditioned media from VEGF challenged HNSCC cells showed a moderate increase in gelatinase activity. Our results demonstrate, for the first time, that HNSCC cells are both targets and effectors for VEGF. These data introduce the prospect that VEGF targeted therapy has the potential to fulfill both anti‐angiogenic and anti‐tumorigenic functions. J. Cell. Biochem. 105: 1202–1210, 2008. © 2008 Wiley‐Liss, Inc.
Secretion of active membrane type 1 matrix metalloproteinase (MMP‐14) into extracellular space in microvesicular exosomes
Authors: Hakulinen Juha , Sankkila Lotta , Sugiyama Nami , Lehti Kaisa , Keski‐Oja Jorma 
Published: September 2008

AbstractMembrane type 1 matrix metalloproteinase (MT1‐MMP, MMP14) is an efficient extracellular matrix (ECM) degrading enzyme that plays important roles in tissue homeostasis and cell invasion. Like a number of type I membrane proteins, MT1‐MMP can be internalized from the cell surface through early and recycling endosomes to late endosomes, and recycled to the plasma membrane. Late endosomes participate in the biogenesis of small (30–100 nm) vesicles, exosomes, which redirect plasma membrane proteins for extracellular secretion. We hypothesized that some of the endosomal MT1‐MMP could be directed to exosomes for extracellular release. Using cultured human fibrosarcoma (HT‐1080) and melanoma (G361) cells we provide evidence that both the full‐length 60 kDa and the proteolytically processed 43 kDa forms of MT1‐MMP are secreted in exosomes. The isolated exosomes were identified by their vesicular structure in electron microscopy and by exosomal marker proteins CD9 and tumor susceptibility gene (TSG101). Furthermore, exosomes contained β1‐integrin (CD29). The exosomes were able to activate pro‐MMP‐2 and degrade type 1 collagen and gelatin, suggesting that the exosomal MT1‐MMP was functionally active. The targeting of MT1‐MMP in exosomes represents a novel mechanism for cancer cells to secrete membrane type metalloproteolytic activity into the extracellular space. J. Cell. Biochem. 105: 1211–1218, 2008. © 2008 Wiley‐Liss, Inc.
Specific signaling cascades involved in cell spreading during healing of micro‐wounded gastric epithelial monolayers
Authors: Tétreault Marie‐Pier , Chailler Pierre , Beaulieu Jean‐François , Rivard Nathalie , Ménard Daniel 
Published: September 2008

AbstractMechanisms that specifically modulate cell spreading and/or cell migration following epithelial wounding are poorly understood. Using micro‐wounded human gastric epithelial monolayers, we show herein that EGF and TGFα maximally increase spreading of epithelial sheets under a cell proliferation‐independent mechanism. Treatment of confluent HGE‐17 cells with the phosphatidylinositol 3‐kinase inhibitor, LY294002, and the epidermal growth factor receptor inhibitor, PD153035, strongly reduced basal and TGFα‐stimulated cell spreading. While pharmacological inhibition of pp60src‐kinase activity also attenuated basal epithelial spreading, addition of the mTOR/p70S6K inhibitor rapamycin or a specific siRNA targeting ILK sequence did not affect the kinetic rates of wound closure. Epithelial wound healing was initiated by actin purse‐string contraction followed by lamellae formation. Conversely, disruption of actin and tubulin stability with cytochalasin D and nocodazole, respectively, inhibited epithelial sheet spreading. Finally, antibodies directed against the α3 integrin subunit, but not against the α6 or α2 subunits, attenuated epithelial sheet spreading as well as lamellae formation. In conclusion, the current investigation establishes that EGF/TGFα and the α3β1 integrin, pp60c‐src, EGFR and PI3K pathways are mainly associated with the cell spreading of the restitution process during healing of human gastric epithelial wounds. J. Cell. Biochem. 105: 1240–1249, 2008. © 2008 Wiley‐Liss, Inc.
Hybridization between Crocodylus acutus and Crocodylus moreletii in the Yucatan Peninsula: II. evidence from microsatellites
Authors: Rodriguez David , Cedeño‐Vázquez José Rogelio , Forstner Michael R. J. , Densmore Llewellyn D. 
Published: September 2008

AbstractDetecting and quantifying hybridization between endangered or threatened taxa can provide valuable information with regards to conservation and management strategies. Hybridization between members of the genus Crocodylus has been known to occur in captivity and in some wild populations. We tested for hybridization among wild populations of American crocodile (C. acutus) and Morelet's crocodile (C. moreletii) in the Yucatan Peninsula by comparing Bayesian assignment tests, based on microsatellite data, to mitochondrial and morphological assignments. Skin clips from 83 individuals were taken for genetic identification, and a total of 32 individuals (38.6%) exhibited some evidence of hybridization by combined morphological, mitochondrial and microsatellite analyses. The majority of hybrids were classified as F2 hybrids and backcrosses to C. moreletii. Most of the introgression occurs in two national biosphere reserves located on the northern and eastern coasts of the Yucatan Peninsula. Preliminary tests did not find a significant decrease in hybridity across three life stages, thus far indicating a low level of selection against hybrids. Model‐based analyses on multilocus genotypes of pure individuals returned little geographic partitioning in both C. acutus and C. moreletii. J. Exp. Zool. 309A:674–686, 2008. © 2008 Wiley‐Liss, Inc.
Probing the limits of molecular imprinting: strategies with a template of limited size and functionality
Authors: Petcu Miruna , Karlsson Jesper G. , Whitcombe Michael J. , Nicholls Ian A. 
Published: September 2008

AbstractA series of polymers molecularly imprinted with the general anaesthetic propofol were synthesized using both semi‐ and non‐covalent approaches. The polymers were evaluated with respect to template rebinding in both aqueous and organic media. In aqueous media, the observed propofol binding in these polymer systems was largely hydrophobic and non‐specific in nature. In non‐polar solvents such as hexane, electrostatic (hydrogen bonding) interactions dominate resulting in some selectivity. The implication of these results, in conjunction with those obtained using structures of similar size in other studies, is that propofol, a template possessing limited functionality and size, appears to define the lower limit for template size and degree of functionalization that can be used for the creation of ligand‐selective recognition sites in molecularly imprinted polymers. Furthermore, studies with alternative ligands indicate that the steric crowding of a ligand's functionality to the polymer contributes to the extent of polymer–ligand recognition. Copyright © 2008 John Wiley & Sons, Ltd.