bluuebunny/crossref_metadata_2025_split huggingface dataset:
Superior Capacitive Performance of Aligned Carbon Nanotubes in Ionic Liquids
Authors: Lu Wen , Qu Liangti , Dai Liming , Henry Kent 
Published: May 2008

Electrodes and electrolytes are two essential components of a supercapacitor and play important roles in determining the performance for the supercapacitor. In the present work, we	investigated the electrochemical and capacitive behavior of aligned carbon nanotube electrodes in ionic liquid electrolytes	to study the feasibility to develop high performance	supercapacitors from these two components. Synthesis procedure of the carbon nanotubes and composition of the ionic liquids	have been studied to achieve a high capacitance and fast charge/discharge process for the carbon nanotube electrode in the ionic liquid electrolyte.
Micro- and Mesoporous Carbon Based Electrode Materials for Electrical Double Layer Capacitors
Authors: Janes Alar , Lust Enn 
Published: May 2008

Micro- and mesoporous carbons are attractive electrode materials with the unique porous structure, narrow pore size distribution	and possibility to fine-tune the pore size for electrodes of electrical double layer capacitors (EDLC), commonly called supercapacitors. The excellent adsorptivity of carbide-derived carbon (CDC) has been demonstrated but these materials are quite expensive and the main aim of this work was to establish conditions for the preparation of nanoporous carbon electrodes,	based on less expensive raw materials, synthesis and activation (i.e. with H2O vapor) methods.
Electrochemical Behavior of Nickel in Acidic Sulfate Electrolytes
Authors: Zangari Giovanni , Villa Marco 
Published: May 2008

The electrochemical behaviour of Nickel in sulphuric acid	electrolytes was studied by various electrochemical means. Under cathodic polarization, Nickel forms metastable hydrides under cathodic charging; the successive egress of hydrogen is controlled by solid state diffusion of hydrogen atoms. The nature of these hydrides evolves with electrochemical aging of the samples, as judged by their electrochemical signature. The nature of the (hydro)oxides formed during anodic polarization also evolves with aging. Anodic polarization and investigation of electrochemical oscillations in the transpassive region show that defect states which constitute preferred dissolution sites assume a wider energy range with increasing aging, indicating a	high degree of inhomogeneity of the surface. The catalytic activity of Nickel increases after aging under both cathodic and anodic conditions, due to the formation of an inhomogeneous surface.
Novel non-Pt PEM Fuel Cell Cathode Catalysts Based on Heteropoly Acid Materials
Authors: Stanis Ronald J. , Kuo Mei Chen , Turner John A. A. , Herring Andrew M. 
Published: May 2008

Heteropoly acids were investigated to determine their activity as non-Pt oxygen reduction reaction (ORR) catalysts in polymer electrolyte membrane fuel cell cathodes (PEMFCs).	Polarization curves, cyclic voltammetry, and impedance spectroscopy results determined that, of the HPAs tested, only Mo based HPAs are active for the ORR and that V substitutions can improve the	activity. Power densities of 67mW at 0.2V were obtained using	H5PMo10V2O40. The catalysts must first be reduced insitu before the HPA can reduce oxygen. The reduction potentials of the HPAs in the fuel cell environment were determined by cyclic voltammetry and provide an explanation for why no activity is seen above 0.55V. Impedance spectroscopy confirmed that V substitutions increase catalytic activity. The potential at which the HPA can be reduced by 4 electrons has been determined to be the limiting factor when using these catalysts for ORR in PEMFCs.
Direct Methane Proton Exchange Membrane Fuel Cell
Authors: Tyagi Sarika , Ganesh Anuradda , Aghalayam Preeti 
Published: May 2008

The direct methane proton exchange membrane fuel cell was	demonstrated for the first time. A Nafion membrane doped with phosphoric acid was used as the electrolyte. Pd/C, Pd-Ru/C and Pd-Au/C were studied as the anode catalysts with catalyst loading of 0.2mg/cm2. Selection of these catalysts for the studies was made based on the activation energy obtained by calculation using the UBI-QEP method. It was shown among these catalysts; Pd-Au/C anode exhibited a maximum open circuit voltage of 0.55V with current density of 30mA/cm2. It was also seen that by bleeding oxygen on anode side, open circuit voltage	was 0.74V and current density was increased to 160mA/cm2.
Carbon Nanotube Electrode Materials for Li-air Cells
Authors: Dai Jinxiang , Kogut Thomas , Jin Lei , Reisner David 
Published: May 2008

In this paper, carbon nanotubes (CNTs) have been investigated as oxygen cathode materials used for Li-oxygen/air cells and compared with carbon black (CB), graphite (G), and active	carbon (AC). Both multi wall nanotube (MWNT) and single wall nanotube (SWNT) showed advantage when compared with other types of carbonaceous materials. The higher discharge capacity of CNTs than AC is explained by the exposed surface area surface area. SWNT is very promising as a cathode material in terms of higher capacity and energy density for Li-oxygen/air cells, while MWNT has low cost advantages. CNT based high energy density Li-oxygen/air cells have the potential to be	developed into high next generation specific energy power sources.
Artesunate Derived from Traditional Chinese Medicine Induces DNA Damage and Repair
Authors: Li Paul C.H. , Lam Elena , Roos Wynand P. , Zdzienicka Małgorzata Z. , Kaina Bernd , Efferth Thomas 
Published: June 2008

Abstract
Artesunate is a semisynthetic derivative from artemisinin, a natural product from the Chinese herb Artemisia annua L. It exerts antimalarial activity, and, additionally, artemisinin and its derivatives are active against cancer cells. The active moiety is an endoperoxide bridge. Its cleavage leads to the formation of reactive oxygen species and carbon-centered radicals. These highly reactive molecules target several proteins in Plasmodia, which is thought to result in killing of the microorganism. DNA damage induced by artemisinins has not yet been described. Here, we show that artesunate induces apoptosis and necrosis. It also induces DNA breakage in a dose-dependent manner as shown by single-cell gel electrophoresis. This genotoxic effect was confirmed by measuring the level of γ-H2AX, which is considered to be an indication of DNA double-strand breaks (DSB). Polymerase β–deficient cells were more sensitive than the wild-type to artesunate, indicating that the drug induces DNA damage that is repaired by base excision repair. irs1 and VC8 cells defective in homologous recombination (HR) due to inactivation of XRCC2 and BRCA2, respectively, were more sensitive to artesunate than the corresponding wild-type. This was also true for XR-V15B cells defective in nonhomologous end-joining (NHEJ) due to inactivation of Ku80. The data indicate that DSBs induced by artesunate are repaired by the HR and NHEJ pathways. They suggest that DNA damage induced by artesunate contributes to its therapeutic effect against cancer cells. [Cancer Res 2008;68(11):4347–51]
CCAAT/Enhancer Binding Protein δ Up-regulates Aromatase Promoters I.3/II in Breast Cancer Epithelial Cells
Authors: Kijima Ikuko , Ye Jingjing , Glackin Carlotta , Chen Shiuan 
Published: June 2008

AbstractAromatase is the enzyme responsible for the last step of estrogen synthesis. The female hormone, estrogen, is known to stimulate breast cancer cell growth. Because the expression of aromatase in breast cancer tissues is driven by unique promoters I.3 and II, a more complete understanding of the regulatory mechanism of aromatase expression through promoters I.3/II in breast tumors should be valuable in developing targeted therapies, which selectively suppress estrogen production in breast tumor tissue. Results from in vivo footprinting analyses revealed several protein binding sites, numbered 1 to 5. When site 2 (−124/−112 bp, exon I.3 start site as +1) was mutated, promoters I.3/II activity was dramatically reduced, suggesting that site 2 is a positive regulatory element. Yeast one-hybrid screening revealed that a potential protein binding to site 2 was CCAAT/enhancer binding protein δ (C/EBPδ). C/EBPδ was shown to bind to site 2 of aromatase promoters I.3/II in vitro and in vivo. C/EBPδ up-regulated promoters I.3/II activity through this site and, as a result, it also up-regulated aromatase transcription and enzymatic activity. p65, a subunit of nuclear factor-κB (NF-κB) transcription factor, inhibited C/EBPδ–up-regulated aromatase promoters I.3/II and enzymatic activity. This inhibitory effect of p65 was mediated, in part, through prevention of the C/EBPδ binding to site 2. This C/EBPδ binding site in aromatase promoters I.3/II seems to act as a positive regulatory element in non–p65-overexpressing breast cancer epithelial cells, whereas it is possibly inactive in p65 overexpressing cancer epithelial cells, such as estrogen receptor–negative breast cancer cells. [Cancer Res 2008;68(11):4455–64]
Long-term In vitro Expansion Alters the Biology of Adult Mesenchymal Stem Cells
Authors: Izadpanah Reza , Kaushal Deepak , Kriedt Christopher , Tsien Fern , Patel Bindiya , Dufour Jason , Bunnell Bruce A. 
Published: June 2008

Abstract
Mesenchymal stem cells (MSC) derived from bone marrow stem cells (BMSC) and adipose tissue stem cells (ASC) of humans and rhesus macaques were evaluated for their cell cycle properties during protracted culture in vitro. Human ASCs (hASC) and rhesus BMSCs (rBMSC) underwent significantly more total population doublings than human BMSCs (hBMSC) and rhesus ASCs (rASC). The cell cycle profile of all MSCs was altered as cultures aged. hMSCs underwent an increase in the frequency of cells in the S phase at P20 and P30. However, rhesus MSCs from both sources developed a distinct polyploid population of cells at P20, which progressed to aneuploidy by P30. Karyotype analysis of MSCs revealed the development of tetraploid or aneuploid karyotypes in the rhesus cells at P20 or P30. Analysis of the transcriptome of the MSCs from early and late passages revealed significant alterations in the patterns of gene expression (8.8% of the genes were differentially expressed in hBMSCs versus hASCs, and 5.5% in rBMSCs versus rASCs). Gene expression changes were much less evident within the same cell type as aging occurred (0.7% in hMSCs and 0.9% in rMSC). Gene ontology analysis showed that functions involved in protein catabolism and regulation of pol II transcription were overrepresented in rASCs, whereas the regulation of IκB/nuclear factor-κB cascade were overrepresented in hBMSCs. Functional analysis of genes that were differentially expressed in rASCs and hBMSCs revealed that pathways involved in cell cycle, cell cycle checkpoints, protein-ubiquitination, and apoptosis were altered. [Cancer Res 2008;68(11):4229–38]
Cells Silenced forSDHBExpression Display Characteristic Features of the Tumor Phenotype
Authors: Cervera Ana M. , Apostolova Nadezda , Crespo Francisco Luna , Mata Manuel , McCreath Kenneth J. 
Published: June 2008

AbstractRecently, enzymes of the tricarboxylic acid (TCA) cycle have emerged as novel tumor suppressors. In particular, mutations in the nuclear-encoded subunits of succinate dehydrogenase (SDHB, SDHC, and SDHD) cause paragangliomas and pheochromocytomas. Although the mechanism(s) by which disruption of mitochondrial metabolism leads to neoplasia is largely unknown, increasing evidence points to an activation of pseudohypoxia. In this study, we have shown that silencing of SDHB using DNA-based small interfering RNA resulted in major impairments in cellular proliferation, respiration, and a corresponding shift to glycolysis. The levels of reactive oxygen species, however, were unchanged. As expected, hypoxia-inducible factor-1α (HIF-1α) and HIF-2α were up-regulated in chronically silenced cells, suggesting that a pseudohypoxic state was attained. In addition, the c-Jun amino-terminal kinase and p38 kinase stress signaling proteins were hyperphosphorylated in SDHB-silenced cells. Microarray analysis showed that &gt;400 genes were influenced (6-fold or more up-regulation or down-regulation) by silencing of SDHB, confirming the importance of the TCA cycle in cellular metabolism. Examples of dysregulated genes included those involved in proliferation, adhesion, and the hypoxia pathway. Of interest, SDHB-silenced cells had a greater capacity to adhere to extracellular matrix components, including fibronectin and laminin, than control cells, thus suggesting a possible mechanism of tumor initiation. Although transient silencing of the HIF-1α transcription factor in SDHB-silenced cells had little effect on the expression of a subset of up-regulated genes, it partially reversed the adhesion phenotype to fibronectin, pointing to a potentially important role for HIF-1 in this process. [Cancer Res 2008;68(11):4058–67]
Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Authors: Lo Roger S. , Witte Owen N. 
Published: June 2008

Abstract
Accumulation of distinct sets of genetic/epigenetic alterations is thought to contribute to stepwise progression of human cutaneous melanomas. We found evidence of frequent tumor cell autonomous transforming growth factor-β (TGF-β) signal activation in both premalignant and malignant stages of human cutaneous melanoma histogenesis and investigated its potential causative roles using human organotypic skin cultures. PTEN deficiency and Braf activation, two common coincident genetic alterations found in primary cutaneous melanomas, were first introduced into human melanocytes previously immortalized by the SV40 large T antigen and telomerase. These changes individually supported anchorage-independent growth and conferred benign, hyperplastic growth in a skin-like environment. In addition, PTEN deficiency combined with Braf activation together induced a melanoma in situ–like phenotype without dermal invasion. Further addition of cell autonomous TGF-β activation in the context of PTEN deficiency and Braf activation promoted dermal invasion in skin cultures without significantly promoting proliferation in vitro and in vivo. This proinvasive phenotype of cell autonomous TGF-β activation is genetic context–dependent, as hyperactivating the TGF-β type I receptor without PTEN deficiency and Braf activation failed to induce an invasive behavior. Evidence of genetic interactions among PTEN deficiency, Braf activation, and cell autonomous TGF-β activation shows that distinct stages of human melanoma are genetically tractable in the proper tissue architecture. [Cancer Res 2008;68(11):4248–57]
Phenotype-Specific CpG Island Methylation Events in a Murine Model of Prostate Cancer
Authors: Camoriano Marta , Morey Kinney Shannon R. , Moser Michael T. , Foster Barbara A. , Mohler James L. , Trump Donald L. , Karpf Adam R. , Smiraglia Dominic J. 
Published: June 2008

Abstract
Aberrant DNA methylation plays a significant role in nearly all human cancers and may contribute to disease progression to advanced phenotypes. Study of advanced prostate cancer phenotypes in the human disease is hampered by limited availability of tissues. We therefore took advantage of the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) model to study whether three different phenotypes of TRAMP tumors (PRIM, late-stage primary tumors; AIP, androgen-independent primary tumors; and MET, metastases) displayed specific patterns of CpG island hypermethylation using Restriction Landmark Genomic Scanning. Each tumor phenotype displayed numerous hypermethylation events, with the most homogeneous methylation pattern in AIP and the most heterogeneous pattern in MET. Several loci displayed a phenotype-specific methylation pattern; the most striking pattern being loci methylated at high frequency in PRIM and AIP but rarely in MET. Examination of the mRNA expression of three genes, BC058385, Goosecoid, and Neurexin 2, which exhibited nonpromoter methylation, revealed increased expression associated with downstream methylation. Only methylated samples showed mRNA expression, in which tumor phenotype was a key factor determining the level of expression. The CpG island in the human orthologue of BC058385 was methylated in human AIP but not in primary androgen-stimulated prostate cancer or benign prostate. The clinical data show a proof-of-principle that the TRAMP model can be used to identify targets of aberrant CpG island methylation relevant to human disease. In conclusion, phenotype-specific hypermethylation events were associated with the overexpression of different genes and may provide new markers of prostate tumorigenesis. [Cancer Res 2008;68(11):4173–82]
Crucial Role of Interleukin-4 in the Survival of Colon Cancer Stem Cells
Authors: Francipane Maria Giovanna , Perez Alea Mileidys , Lombardo Ylenia , Todaro Matilde , Medema J.P. , Stassi Giorgio 
Published: June 2008

Abstract
Colon tumors may be maintained by a rare fraction of cancer stem-like cells (CSC) that express the cell surface marker CD133. Self-renewing CSCs exhibit relatively greater resistance to clinical cytotoxic therapies and recent work suggests that this resistance may be mediated in part by an autocrine response to the immune cytokine interleukin 4 (IL-4). Blocking IL-4 signaling can sensitize CSCs to apoptotic stimuli and increase the in vivo efficacy of cytotoxic therapy. These findings suggest that inhibitors of IL-4 signaling may offer a new therapeutic tool in colon carcinoma. [Cancer Res 2008;68(11):4022–5]
Involvement of Rac in Fenretinide-Induced Apoptosis
Authors: Kadara Humam , Tahara Eiji , Kim Hyun-Jung , Lotan Dafna , Myers Jeffrey , Lotan Reuben 
Published: June 2008

Abstract
The synthetic retinoid N-(4-hydroxyphenyl)retinamide (4HPR) has shown potential as a chemopreventive and therapeutic agent. The ability of 4HPR to enhance production of reactive oxygen species (ROS) leading to apoptosis has been suggested as a possible mechanism underlying these effects. We explored the possibility that ROS induction by 4HPR involves the small GTPase Ras-related C3 botulinum toxin substrate (Rac), a regulatory subunit of the NADPH oxidase complex. Rac was activated in human head and neck squamous cell carcinoma (HNSCC) cells as early as 5 minutes following 4HPR exposure. Moreover, inhibition of Rac activity or silencing of its expression by RNA interference decreased ROS generation in human head and neck, lung, and cervical cancer cells and murine melanoma cells. In HNSCC UMSCC-22B cells, this decrease correlated with reduction in apoptosis induction by 4HPR. Expression of a constitutive active mutant Rac increased basal and 4HPR-induced ROS generation and poly(ADP-ribose) polymerase cleavage. In addition, the metastatic DM14 cells exhibited higher Rac activation following 4HPR treatment compared with the primary Tu167-C2 cells. Furthermore, the metastatic cancer cells tested exhibited higher ROS generation and growth inhibition due to 4HPR exposure compared with their primary cancer cell counterparts. These findings show a preferential susceptibility of metastatic cells to the proapoptotic retinoid 4HPR through Rac activation and support the use of ROS-inducing agents such as 4HPR against metastatic cancer cells. [Cancer Res 2008;68(11):4416–23]
Histone Deacetylase Inhibitors Reverse SS18-SSX–Mediated Polycomb Silencing of the Tumor Suppressor Early Growth Response 1 in Synovial Sarcoma
Authors: Lubieniecka Joanna M. , de Bruijn Diederik R.H. , Su Le , van Dijk Anke H.A. , Subramanian Subbaya , van de Rijn Matt , Poulin Neal , van Kessel Ad Geurts , Nielsen Torsten O. 
Published: June 2008

Abstract
Synovial sarcoma is a soft tissue malignancy characterized by the fusion of SS18 to either SSX1, SSX2, or SSX4 genes. SS18 and SSX are transcriptional cofactors involved in activation and repression of gene transcription, respectively. SS18 interacts with SWI/SNF, whereas SSX associates with the polycomb chromatin remodeling complex. Thus, fusion of these two proteins brings together two opposing effects on gene expression and chromatin structure. Recent studies have shown that a significant number of genes are down-regulated by the SS18-SSX fusion protein and that the clinically applicable histone deacetylase (HDAC) inhibitor romidepsin inhibits synovial sarcoma growth. Therefore, we set out to identify direct targets of SS18-SSX among genes down-regulated in synovial sarcoma and investigated if romidepsin can specifically counteract SS18-SSX–mediated transcriptional dysregulation. Here, we report that the tumor suppressor early growth response 1 (EGR1) is repressed by the SS18-SSX protein through a direct association with the EGR1 promoter. This SS18-SSX binding correlates with trimethylation of Lys27 of histone H3 (H3K27-M3) and recruitment of polycomb group proteins to this promoter. In addition, we found that romidepsin treatment reverts these modifications and reactivates EGR1 expression in synovial sarcoma cell models. Our data implicate polycomb-mediated epigenetic gene repression as a mechanism of oncogenesis in synovial sarcoma. Furthermore, our work highlights a possible mechanism behind the efficacy of a clinically applicable HDAC inhibitor in synovial sarcoma treatment. [Cancer Res 2008;68(11):4303–10]
Carcinoma-Associated Fibroblast–Like Differentiation of Human Mesenchymal Stem Cells
Authors: Mishra Pravin J. , Mishra Prasun J. , Humeniuk Rita , Medina Daniel J. , Alexe Gabriela , Mesirov Jill P. , Ganesan Sridhar , Glod John W. , Banerjee Debabrata 
Published: June 2008

Abstract
Carcinoma-associated fibroblasts (CAF) have recently been implicated in important aspects of epithelial solid tumor biology, such as neoplastic progression, tumor growth, angiogenesis, and metastasis. However, neither the source of CAFs nor the differences between CAFs and fibroblasts from nonneoplastic tissue have been well defined. In this study, we show that human bone marrow–derived mesenchymal stem cells (hMSCs) exposed to tumor-conditioned medium (TCM) over a prolonged period of time assume a CAF-like myofibroblastic phenotype. More importantly, these cells exhibit functional properties of CAFs, including sustained expression of stromal-derived factor-1 (SDF-1) and the ability to promote tumor cell growth both in vitro and in an in vivo coimplantation model, and expression of myofibroblast markers, including α-smooth muscle actin and fibroblast surface protein. hMSCs induced to differentiate to a myofibroblast-like phenotype using 5-azacytidine do not promote tumor cell growth as efficiently as hMSCs cultured in TCM nor do they show increased SDF-1 expression. Furthermore, gene expression profiling revealed similarities between TCM-exposed hMSCs and CAFs. Taken together, these data suggest that hMSCs are a source of CAFs and can be used in the modeling of tumor-stroma interactions. To our knowledge, this is the first report showing that hMSCs become activated and resemble carcinoma-associated myofibroblasts on prolonged exposure to conditioned medium from MDAMB231 human breast cancer cells. [Cancer Res 2008;68(11):4331–9]