bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mouse mammary tumor virus‐like env sequences in human breast cancer
Authors: Mok Myth T.S. , Lawson James S. , Iacopetta Barry J. , Whitaker Noel J. 
Published: March 2008

AbstractMouse mammary tumor virus (MMTV) has long been known as a causal agent of breast cancer in mice. To date, varied MMTV‐like envelope gene (env) sequences have been identified in up to 74% of human breast cancers. However, the role and origin of these MMTV‐like sequences in human breast cancer remain uncertain. Our study was initiated to study the integration of MMTV‐like env sequences in human breast cancer. PCR screening has identified 28 (56%) Australian breast cancer specimens and 7 (87.5%) human breast cancer cell lines to be positive for MMTV‐like env sequence. In the MCF‐7 genome, a fragment containing an MMTV‐like env sequence of ∼1.9 kb plus a downstream rodent‐like sequence of ∼200 bp was found to be integrated into a bacterial‐like β‐lactamase sequence by insertional mutagenesis. The identified MMTV‐rodent fragment is present in some MCF‐7 sublines but absent in the screened specimens and other cell lines. Sporadic mutations found in this fragment indicate it has multiple copies in the MCF‐7 genome. Sequence analysis has identified a novel ORF of ∼1.6 kb which is 94–99% identical to MMTV env genes. RT‐PCR was performed on the MCF‐7 cDNA but no MMTV‐like env transcript was detected. This is the first report to reveal the locus of MMTV‐like env sequence in human cells. The MMTV‐like env sequence was shown to be distinct from the human endogenous retroviral sequences and is closely related to rodents. © 2008 Wiley‐Liss, Inc.
Protective role of 1α, 25‐dihydroxyvitamin D3 against oxidative stress in nonmalignant human prostate epithelial cells
Authors: Bao Bo‐Ying , Ting Huei‐Ju , Hsu Jong‐Wei , Lee Yi‐Fen 
Published: March 2008

AbstractOverproduction of reactive oxygen species (ROS), through either endogenous or exogenous sources, could induce DNA damage, and accumulation of DNA damage might lead to multistep carcinogenesis. The antioxidative effects of vitamin D have been suggested by epidemiological and many in vitro and in vivo laboratory studies. While exploring the antioxidative effects of vitamin D in prostate cells, we found that the active form of vitamin D, 1α, 25‐dihydroxyvitamin D3 (1,25‐VD), can protect nonmalignant human prostate epithelial cell lines, BPH‐1 and RWPE‐1, but not malignant human prostate epithelial cells, CWR22R and DU 145, from oxidative stress‐induced cell death. Glucose‐6‐phosphate dehydrogenase (G6PD), a key antioxidant enzyme, was dose‐ and time‐dependently induced by 1,25‐VD. Mechanistic studies using chromatin immunoprecipitation (ChIP) assay revealed that a direct repeat‐3 (DR3) vitamin D response element located in the first intron of the G6PD genome can be bound by liganded vitamin D receptor, thereby regulating G6PD gene expression. Increasing G6PD activity and glutathione level by 1,25‐VD can scavenge cellular ROS. Moreover, the protective effects of 1,25‐VD were abolished by dehydroepiandrosterone, a noncompetitive inhibitor of G6PD activity. Together, our results showed that 1,25‐VD can protect nonmalignant prostate cells from oxidative stress‐induced cell death by elimination of ROS‐induced cellular injuries through transcriptional activation of G6PD activity. The antioxidative effect of vitamin D strengthens its roles in cancer chemoprevention and adds to a growing list of beneficial effects of vitamin D against cancer. © 2008 Wiley‐Liss, Inc.
Expression and localization of estrogen receptor α in the C2C12 murine skeletal muscle cell line
Authors: Milanesi Lorena , de Boland Ana Russo , Boland Ricardo 
Published: March 2008

AbstractThe classical model of 17β‐estradiol action has been traditionally described to be mediated by the estrogen receptor (ER) localized exclusively in the nucleus. However, there is increasing functional evidence for extra nuclear localization of ER. We present biochemical, immunological and molecular data supporting mitochondrial‐microsomal localization of ERα in the C2C12 skeletal muscle cell line. We first established [3H]17βestradiol binding characteristics in whole cells in culture. Specific and saturable [3H]17βestradiol binding sites of high affinity were then detected in mitochondrial fractions (Kd = 0.43 nM; Bmax = 572 fmol/mg protein). Immunocytological studies revealed that estrogen receptors mainly localize at the mitochondrial and perinuclear level. These results were also confirmed using fluorescent 17βestradiol‐BSA conjugates. The immunoreactivity did not translocate into the nucleus by 17β‐estradiol treatment. Western and Ligand blot approaches corroborated the non‐classical localization. Expression and subcellular distribution of ERα proteins were confirmed in C2C12 cells transfected with ERα siRNA and by RT‐PCR employing specific primers. The non‐classical distribution of native pools of ERα in skeletal muscle cells suggests an alternative mode of ER localization/function. J. Cell. Biochem. 104: 1254–1273, 2008. © 2008 Wiley‐Liss, Inc.
Non‐enzymatic glycation of type I collagen diminishes collagen–proteoglycan binding and weakens cell adhesion
Authors: Reigle Kristin L. , Di Lullo Gloria , Turner Kevin R. , Last Jerold A. , Chervoneva Inna , Birk David E. , Funderburgh James L. , Elrod Elizabeth , Germann Markus W. , Surber Charles , Sanderson Ralph D. , San Antonio James D. 
Published: March 2008

AbstractNon‐enzymatic glycation of type I collagen occurs in aging and diabetes, and may affect collagen solubility, charge, polymerization, and intermolecular interactions. Proteoglycans1 (PGs) bind type I collagen and are proposed to regulate fibril assembly, function, and cell–collagen interactions. Moreover, on the collagen fibril a keratan sulfate (KS) PG binding region overlaps with preferred collagen glycation sites. Thus, we examined the effect of collagen modified by simple glycation on PG–collagen interactions. By affinity coelectrophoresis (ACE), we found reduced affinities of heparin and KSPGs for glycated but not normal collagen, whereas the dermatan sulfate (DS)PGs decorin and biglycan bound similarly to both, and that the affinity of heparin for normal collagen decreased with increasing pH. Circular dichroism (CD) spectroscopy revealed normal and glycated collagens to assume triple helical conformations, but heparin addition caused precipitation and decreased triple helical content—effects that were more marked with glycated collagen. A spectrophotometric assay revealed slower polymerization of glycated collagen. However, ultrastructural analyses indicated that fibrils assembled from normal and glycated collagen exhibited normal periodicity, and had similar structures and comparable diameter distributions. B‐cells expressing the cell surface heparan sulfate PG syndecan‐1 adhered well to normal but not glycated collagen, and endothelial cell migration was delayed on glycated collagen. We speculate that glycation diminishes the electrostatic interactions between type I collagen and PGs, and may interfere with core protein‐collagen associations for KSPGs but not DSPGs. Therefore in vivo, collagen glycation may weaken PG–collagen interactions, thereby disrupting matrix integrity and cell–collagen interactions, adhesion, and migration. J. Cell. Biochem. 104: 1684–1698, 2008. © 2008 Wiley‐Liss, Inc.
CBF/NF‐Y controls endoplasmic reticulum stress induced transcription through recruitment of both ATF6(N) and TBP
Authors: Luo Rong , Lu Jing‐Fang , Hu Qianghua , Maity Sankar N. 
Published: March 2008

AbstractPreviously the analysis of promoters regulated by endoplasmic reticulum (ER) stress identified a composite promoter element, ERSE that interacts with both CBF/NF‐Y (CBF) and ATF6(N) transcription factors. This prompted us to investigate the underlying mechanism by which CBF, a ubiquitously binding transcription factor, specifically controls transcription activation during ER stress. The in vitro DNA binding study performed using purified recombinant proteins revealed that CBF specifically recruits ATF6(N) to ERSE DNA but it does not interact with ATF6(N) in absence of DNA binding. Inhibition of CBF binding resulted in a significant reduction of optimal transcription activation of cellular genes during ER stress. Analysis of cellular promoters by ChIP demonstrated that CBF is needed for recruitment of both ATF6(N) and TBP but not for either acetylation of histone H3‐K9 or trimethylation of histone H3‐K4 during ER stress. Together these study results reveal that CBF controls ER stress‐inducible transcription through recruitment of both ATF6(N) and TBP but not through chromatin modifications. Our observations are in agreement with the results of recently published studies that have shown that CBF controls transcription of varieties of inducible promoters through recruitment of general transcription factors but not through acetylation of histone H4. These findings provide a paradigm of the function of CBF in inducible transcription. J. Cell. Biochem. 104: 1708–1723, 2008. © 2008 Wiley‐Liss, Inc.
Differential regulation of mTOR‐dependent S6 phosphorylation by muscarinic acetylcholine receptor subtypes
Authors: Slack Barbara E. , Blusztajn Jan K. 
Published: March 2008

AbstractMuscarinic receptors subserve many functions in both peripheral and central nervous systems. Some of these processes depend on increases in protein synthesis, which may be achieved by activation of mammalian target of rapamycin (mTOR), a kinase that regulates protein translation capacity. Here, we examined the regulation of mTOR‐dependent signaling pathways by muscarinic receptors in SK‐N‐SH human neuroblastoma cells, and in human embryonic kidney (HEK) cell lines transfected with individual muscarinic receptor subtypes. In SK‐N‐SH cells, the acetylcholine analog carbachol stimulated phosphorylation of the ribosomal S6 protein, a downstream target of mTOR. The sensitivity of the response to subtype‐selective muscarinic receptor antagonists indicated that it was mediated by M3 receptors. Carbachol‐evoked S6 phosphorylation was blocked by the mTOR inhibitor rapamycin, but was independent of phosphoinositide 3‐kinase activation. The response was significantly reduced by the mitogen‐activated protein kinase kinase (MEK) inhibitor U0126, which also inhibited carbachol‐evoked S6 phosphorylation in HEK cells expressing M2 receptors, but was ineffective in M3 receptor‐expressing HEK cells, although carbachol activated MAPK in both transfected lines. The p90 ribosomal S6 kinase has been implicated in mTOR regulation by phorbol esters, but was not activated by carbachol in any of the cell lines tested. The protein kinase C inhibitor bisindolylmaleimide I reduced carbachol‐stimulated S6 phosphorylation in SK‐N‐SH cells, and in HEK cells expressing M3 receptors, but not in HEK cells expressing M2 receptors. The results demonstrate that multiple muscarinic receptor subtypes regulate mTOR, and that both MAPK‐dependent and ‐independent mechanisms may mediate the response in a cell context‐specific manner. J. Cell. Biochem. 104: 1818–1831, 2008. © 2008 Wiley‐Liss, Inc.
PEDF from mouse mesenchymal stem cell secretome attracts fibroblasts
Authors: Sarojini Harshini , Estrada Rosendo , Lu Hongwei , Dekova Silvia , Lee Menq‐Jer , Gray Robert D. , Wang Eugenia 
Published: March 2008

AbstractConditioned medium (secretome) derived from an enriched stem cell culture stimulates chemotaxis of human fibroblasts. These cells are classified as multipotent murine mesenchymal stromal cells (mMSC) by immunochemical analysis of marker proteins. Proteomic analysis of mMSC secretome identifies nineteen secreted proteins, including extracellular matrix structural proteins, collagen processing enzymes, pigment epithelium‐derived factor (PEDF) and cystatin C. Immunodepletion and reconstitution experiments show that PEDF is the predominant fibroblast chemoattractant in the conditioned medium, and immunofluorescence microscopy shows strong staining for PEDF in the cytoplasm, at the cell surface, and in intercellular space between mMSCs. This stimulatory effect of PEDF on fibroblast chemotaxis is in contrast to the PEDF‐mediated inhibition of endothelial cell migration, reported previously. These differential functional effects of PEDF toward fibroblasts and endothelial cells may serve to program an ordered temporal sequence of scaffold building followed by angiogenesis during wound healing. J. Cell. Biochem. 104: 1793–1802, 2008. © 2008 Wiley‐Liss, Inc.
DNA damage, RAD9 and fertility/infertility of Echinococcus granulosus hydatid cysts
Authors: Cabrera Gonzalo , Cabrejos María Eugenia , Morassutti Alessandra Loureiro , Cabezón Carolina , Orellana Juana , Hellman Ulf , Zaha Arnaldo , Galanti Norbel 
Published: March 2008

AbstractHydatidosis, caused by the larval stage of the platyhelminth parasite Echinococcus granulosus, affects human and animal health. Hydatid fertile cysts are formed in intermediate hosts (human and herbivores) producing protoscoleces, the infective form to canines, at their germinal layers. Infertile cysts are also formed, but they are unable to produce protoscoleces. The molecular mechanisms involved in hydatid cysts fertility/infertility are unknown. Nevertheless, previous work from our laboratory has suggested that apoptosis is involved in hydatid cyst infertility and death. On the other hand, fertile hydatid cysts can resist oxidative damage due to reactive oxygen and nitrogen species. On these foundations, we have postulated that when oxidative damage of DNA in the germinal layers exceeds the capability of DNA repair mechanisms, apoptosis is triggered and hydatid cysts infertility occurs. We describe a much higher percentage of nuclei with oxidative DNA damage in dead protoscoleces and in the germinal layer of infertile cysts than in fertile cysts, suggesting that DNA repair mechanisms are active in fertile cysts. rad9, a conserved gene, plays a key role in cell cycle checkpoint modulation and DNA repair. We found that RAD9 of E. granulosus (EgRAD9) is expressed at the mRNA and protein levels. As it was found in other eukaryotes, EgRAD9 is hyperphosphorylated in response to DNA damage. Our results suggest that molecules involved in DNA repair in the germinal layer of fertile hydatid cysts and in protoscoleces, such as EgRAD9, may allow preserving the fertility of hydatid cysts in the presence of ROS and RNS. J. Cell. Physiol. 216: 498–506, 2008. © 2008 Wiley‐Liss, Inc.
Adenovirus E1A oncoprotein liberates c‐Myc activity to promote cell proliferation through abating Bin1 expression via an Rb/E2F1‐dependent mechanism
Authors: Kinney Erica L. , Tanida Satoshi , Rodrigue Amelie A. , Johnson Joanna K. , Tompkins Van S. , Sakamuro Daitoku 
Published: March 2008

AbstractAdenovirus E1A oncogene transforms primary rodent fibroblasts in cooperation with activated Ras. Conversely, the c‐Myc oncoprotein‐binding tumor suppressor, Bin1, inhibits Ras/E1A‐mediated cell transformation. Since E1A does not directly bind to and inhibit Bin1, the primary mechanism by which E1A counteracts Bin1 to liberate oncogenic c‐Myc activity is poorly understood. Here we show that wild‐type E1A, but not an Rb binding‐defective E1A mutant, suppresses endogenous Bin1 expression in cultured rodent fibroblasts. Similarly, other anti‐Rb agents, such as human papillomavirus E7, mitogenic stimuli, and small interfering RNA (siRNA) for Rb, consistently decrease Bin1 promoter activity. In contrast, serum starvation, which activates Rb, enhances endogenous Bin1 levels. These findings suggest that Bin1 may be a novel component of Rb‐mediated G1 arrest. Consistent with this premise, chromatin immunoprecipitation assays demonstrate that Rb protein directly interacts with the Bin1 promoter only upon removal of serum. Furthermore, ectopically expressed E2F1, which is primarily inhibited by Rb under serum‐starved condition, represses Bin1 promoter activity in a manner that is dependent on the DNA‐binding and transactivation domains of E2F1. Lastly, depletion of endogenous Bin1 per se is biologically meaningful since antisense or siRNA of Bin1 transfection releases endogenous c‐Myc transcriptional activity and, concomitantly, accelerates cell proliferation. Our results suggest that Bin1 gene suppression caused by oncogenic E1A via Rb inactivation is an essential step in cell cycle progression promoted by c‐Myc, and subsequently, E1A transformation. We propose a novel G1 arrest signaling mechanism by which Rb indirectly curbs oncogenic c‐Myc activity via sustaining Bin1 expression. J. Cell. Physiol. 216: 621–631, 2008, © 2008 Wiley‐Liss, Inc.
Synthesis and Raman spectroscopic characterisation of the oxalate mineral wheatleyite Na2Cu2+(C2O4)2·2H2O
Authors: Frost Ray L. , Locke Ashley , Martens Wayde N. 
Published: March 2008

AbstractThe mineral wheatleyite has been synthesised and characterised by Raman spectroscopy complimented with infrared spectroscopy. Two Raman bands at 1434 and 1470 cm−1 are assigned to the ν(CO) stretching mode and implies two independent oxalate anions. Two intense Raman bands observed at 904 and 860 cm−1 are assigned to the ν(CC) stretching mode and support the concept of two non‐equivalent oxalate units in the wheatleyite structure. Two strong bands observed at 565 and 585 cm−1 are assigned to the symmetric CCO in plane bending modes. The Raman band at 387 cm−1 is attributed to the CuO stretching vibration and the bands at 127 and 173 cm−1 to OCuO bending vibrations. A comparison is made with Raman spectra of selected natural oxalate bearing minerals. Oxalates are markers or indicators of environmental events. Oxalates are readily determined by Raman spectroscopy. Thus, deterioration of works of art, biogeochemical cycles, plant metal complexation, the presence of pigments and minerals formed in caves can be analysed. Copyright © 2008 John Wiley & Sons, Ltd.
A new limb salvage surgery in cases of high‐grade soft tissue sarcoma using photodynamic surgery, followed by photo‐ and radiodynamic therapy with acridine orange
Authors: Nakamura Tomoki , Kusuzaki Katsuyuki , Matsubara Takao , Matsumine Akihiko , Murata Hiroaki , Uchida Atsumasa 
Published: March 2008

AbstractBackgroundTo maintain excellent limb function after tumor resection in patients with high‐grade malignant sarcomas, we developed and established a new surgical adjuvant therapy using acridine orange (AO) after intra‐lesional or marginal resection while sparing normal tissues of major nerves, vessels or bones adjacent to the tumor.MethodOur AO therapy procedure was combined with photodynamic surgery (PDS), photodynamic therapy (PDT) and radiodynamic therapy (RDT). In this study, 26 patients with primary high‐grade soft tissue sarcomas were treated with AO therapy.ResultResults showed a low local recurrence rate (7.7%) and good local recurrence‐free rate (88%) after AO therapy. Limb function of all patients was maintained at 100% of ISOLS criteria.ConclusionBased on these results, we concluded that AO therapy is useful for local control after margin‐positive tumor resection and for preserving excellent limb function in patients with high‐grade soft tissue sarcomas. J. Surg. Oncol. 2008;97:523–528. © 2008 Wiley‐Liss, Inc.
Identification of protein‐coding and intronic noncoding RNAs down‐regulated in clear cell renal carcinoma
Authors: Brito Glauber Costa , Fachel Ângela A. , Vettore Andre Luiz , Vignal Giselle M , Gimba Etel R.P. , Campos Franz S. , Barcinski Marcello A. , Verjovski‐Almeida Sergio , Reis Eduardo M. 
Published: March 2008

AbstractThe clear cell subtype of renal cell carcinoma (RCC) is the most lethal and prevalent cancer of the urinary system. To investigate the molecular changes associated with malignant transformation in clear cell RCC, the gene expression profiles of matched samples of tumor and adjacent non‐neoplastic tissue were obtained from six patients. A custom‐built cDNA microarray platform was used, comprising 2292 probes that map to exons of genes and 822 probes for noncoding RNAs mapping to intronic regions. Intronic transcription was detected in all normal and neoplastic renal tissues. A subset of 55 transcripts was significantly down‐regulated in clear cell RCC relative to the matched nontumor tissue as determined by a combination of two statistical tests and leave‐one‐out patient cross‐validation. Among the down‐regulated transcripts, 49 mapped to untranslated or coding exons and 6 were intronic relative to known exons of protein‐coding genes. Lower levels of expression of SIN3B, TRIP3, SYNJ2BP and NDE1 (P < 0.02), and of intronic transcripts derived from SND1 and ACTN4 loci (P < 0.05), were confirmed in clear cell RCC by Real‐time RT‐PCR. A subset of 25 transcripts was deregulated in additional six nonclear cell RCC samples, pointing to common transcriptional alterations in RCC irrespective of the histological subtype or differentiation state of the tumor. Our results indicate a novel set of tumor suppressor gene candidates, including noncoding intronic RNAs, which may play a significant role in malignant transformations of normal renal cells. © 2008 Wiley‐Liss, Inc.
Distributive smoothers in multigrid for problems with dominating grad–div operators
Authors: Gaspar F. J. , Gracia J. L. , Lisbona F. J. , Oosterlee C. W. 
Published: March 2008

AbstractIn this paper, we present efficient multigrid methods for systems of partial differential equations that are governed by a dominating grad–div operator. In particular, we show that distributive smoothing methods give multigrid convergence factors that are independent of problem parameters and of the mesh sizes in space and time. The applications range from model problems to secondary consolidation Biot's model. We focus on the smoothing issue and mainly solve academic problems on Cartesian‐staggered grids. Copyright © 2008 John Wiley & Sons, Ltd.
Epoxy resin/plasticized carbon black composites. Part I. Electrical and thermal properties and their applications
Authors: Abdel‐Aal N. , El‐Tantawy Farid , Al‐Hajry A. , Bououdina M. 
Published: March 2008

AbstractThe development of conductive polymer composites remains an important endeavor in light of growing energy concerns. A conducting polymer composite in the presence of plasticized carbon black (CB) and epoxy resin has been developed. Room temperature electrical conductivity, mobility carriers (μ), and number of charges (N) increase by increasing CB content. Electrical conductivity–temperature dependence of the composite was investigated and negative temperature coefficient of conductivity (NTC) behavior of the composites was revealed. The mechanism of the NTC effect in materials is related to the thermal expansion of the epoxy matrix and barriers height energy. The current–voltage behavior of epoxy/CB composites shows a switching effect and the mechanism of negative resistance is interpreted in details. Thermal conductivity (γ) increases with increasing filler content and the experimental data was compared with a theoretical model based on energy balance equation. POLYM. COMPOS., 2008. © 2008 Society of Plastics Engineers