bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ti‐Catalyzed Barbier‐Type Allylations and Related Reactions
Authors: Estévez Rosa E. , Justicia José , Bazdi Btissam , Fuentes Noelia , Paradas Miguel , Choquesillo‐Lazarte Duane , García‐Ruiz Juan M. , Robles Rafael , Gansäuer Andreas , Cuerva Juan M. , Oltra J. Enrique 
Published: January 2009

AbstractVersatility of titanium: Titanocene(III) complexes catalyze Barbier‐type allylations, intramolecular crotylations (cyclizations), and prenylations of a wide range of aldehydes and ketones. These reactions take place at RT under mild conditions compatible with many functional groups; provide good yields of open‐chain and cyclic homoallylic alcohols, including heterocyclic derivatives; and can be conducted enantioselectively by using enantiomerically pure titanium catalysts.magnified imageTitanocene(III) complexes, easily generated in situ from commercial TiIV precursors, catalyze Barbier‐type allylations, intramolecular crotylations (cyclizations), and prenylations of a wide range of aldehydes and ketones. The reaction displays surprising and unprecedented mechanistic subtleties. In cyclizations a fast and irreversible addition of an allyl radical to a TiIII‐coordinated carbonyl group seems to occur. Intermolecular additions to conjugated aldehydes proceed through a coupling of a TiIV‐bound ketyl radical with an allyl radical. Reactions of ketones with allylic halides take place by the classical addition of an allylic organometallic reagent. The radical coupling processes enable transformations such as the highly regioselective α‐prenylation that are otherwise difficult to achieve. The mild reaction conditions and the possibility to employ titanocene complexes in only catalytic quantities are highly attractive features of our protocol. These unusual properties have been taken advantage of for the straightforward synthesis of the natural products rosiridol, shikalkin, and 12‐hydroxysqualene.
The effect of mismatch in current‐versusvoltage‐mode resistive grids
Authors: Shi Bertram E. 
Published: January 2009

AbstractResistive grids are commonly used in neuromorphic very large‐scale integration (VLSI) designs for image smoothing and signal aggregation. Because mismatch is inevitable in VLSI chips, one reason that resistive grids are attractive is that their output is robust to mismatch in the component values. Here, we examine relative sensitivity of different resistive grid designs that differ depending upon whether the input and output are represented by current or voltage. Our analysis reveals that a mixed‐mode design, where the input is represented by current but the output is represented by voltage, is less sensitive to mismatch when the amount of smoothing is large. On the other hand, when little smoothing is desired, pure voltage‐mode and current‐mode designs are preferred. From the point of view of mismatch sensitivity, there is little difference between the two pure‐mode designs. Our analysis also reveals that the difference in mismatch sensitivity is due to the vertical resistors, which are the most sensitive to mismatch in all the three designs studied. Copyright © 2008 John Wiley & Sons, Ltd.
Investigation of a DNA‐Based Biosensor with Chitosan‐Carbon Nanotubes Interface by Cyclic and Elimination Voltammetry
Authors: Galandova Julia , Trnkova Libuse , Mikelova Radka , Labuda Jan 
Published: January 2009

AbstractThe paper presents a disposable DNA biosensor based on a composite of multiwalled carbon nanotubes (MWCNT) in chitosan (CHIT) used as an interface at the screen printed carbon electrode (SPCE). Double stranded herring sperm DNA was immobilized over the MWCNT‐CHIT layer. The response of the modified SPCE with and without DNA was characterized using the redox probe [Fe(CN)6]3−/4− in the mode of cyclic voltammetry and elimination voltammetry with linear scan (EVLS), which enables the elimination of selected partial voltammetric currents contributing to the total current. The elimination functions providing a significant increase in the voltammetric current sensitivity and improving the peak resolution enable to indicate an adsorbed state of depolarizers, to discover hidden electrode processes, and to determine their nature. The SPCE surface modification was evaluated using (a) the charge transfer coefficient α of the redox probe calculated from the Tafel plot analysis (TPA) and EVLS and (b) the polarization resistance RP for both cathodic and anodic processes.
Bismuth‐Coated Screen‐Printed Microband Electrodes for On‐Field Labile Cadmium Determination
Authors: Zaouak Olivier , Authier Laurent , Cugnet Cyril , Castetbon Alain , Potin‐Gautier Martine 
Published: January 2009

AbstractPerformances of a screen‐printed microband electrode prepared by ex situ bismuth deposition are reported. According to the low bismuth toxicity, this electrode represents an environmentally friendly alternative to mercury modified sensors, particularly for on‐field measurements. The electrochemical behaviour of the microband electrode has been studied and is in agreement with microelectrode theory before and after bismuth modification. Sensitive cadmium analysis achieved in nondeaerated and unstirred solutions leads to a detection limit of 1.3 μg L−1 using SWASV for 120 s deposition time. This sensor has been successfully applied to a nontreated river water sample.
Zinc hydroxystannate‐coated metal hydroxides as flame retardant and smoke suppression for flexible poly vinyl chloride
Authors: Qu Hongqiang , Wu Weihong , Xie Jixing , Xu Jianzhong 
Published: January 2009

AbstractZinc hydroxystannate (ZHS)‐coated metal hydroxides were prepared. The effects of ZHS‐coated metal hydroxides on flame retardancy and smoke suppression of flexible poly vinyl chloride were studied by means of the limiting oxygen index, smoke density rating and the char yield test. The mechanism was investigated by thermogravimerty (TG), differential thermal analysis, and differential TG analysis and scanning electron microscopy. The results showed that ZHS‐coated metal hydroxides are more effective flame retardant and smoke suppressant than metal hydroxides, and it appears that tin compound may exert its action in both the condensed and vapor phases, but mainly in condensed phases as a Lewis acid. Copyright © 2009 John Wiley & Sons, Ltd.
Alpha fetoprotein is a novel protein‐binding partner for caspase‐3 and blocks the apoptotic signaling pathway in human hepatoma cells
Authors: Li Mengsen , Li Hui , Li Chaoying , Zhou Sheng , Guo Liyuan , Liu Han , Jiang Wei , Liu Xinhua , Li Pingfeng , McNutt Michael A. , Li Gang 
Published: January 2009

AbstractAlthough there is increasing evidence that alpha fetoprotein (AFP) may function as regulatory factor in the growth of tumor cells, the precise mechanism is still unclear. In the current study, we investigated the role of the cytoplasmic AFP in caspase‐3‐mediated signaling of apoptosis. Our results showed that low doses of TNF‐related apoptosis‐inducing ligand (TRAIL) elevated the activity of caspase‐8, but not caspase‐3. Caspase‐3 colocalized and interacted with AFP in the cytoplasm of Bel 7402 cells, and translocated into nuclei in association with the occurrence of apoptosis while cells were under cotreatment with all‐trans retinoic acid (ATRA) or TRAIL. AFP was able to form complexes with caspase‐3 and block onward transmission of signaling from caspase‐8. Knockdown of AFP increased the sensitivity of Bel 7402 cells to TRAIL, and thereby, triggered caspase‐3 signaling. No intermolecule interaction occurred between AFP and caspase‐8, nor was caspase‐8 activity altered after AFP knockdown, demonstrating the selectivity of AFP in interfering with the apoptotic signaling pathway. The effect of AFP on caspase‐3 was further confirmed by transfection of the AFP gene into HLE cells (AFP negative). We conclude that ATRA or TRAIL resistance in AFP producing hepatoma is at least, in part, attributable to the high level of the cytoplasmic AFP. Therefore, it is possible that the combination of AFP gene silencing together with ATRA/TRAIL cotreatment will benefit the enhancement of the chemotherapeutic efficiency of these agents on tumors. © 2009 UICC
Nmi (N‐Myc interactor) inhibits Wnt/β‐catenin signaling and retards tumor growth
Authors: Fillmore Rebecca A. , Mitra Aparna , Xi Yaguang , Ju Jingfang , Scammell Jonathan , Shevde Lalita A. , Samant Rajeev S. 
Published: January 2009

AbstractWe found that the expression levels of N‐Myc interactor (Nmi) were low in aggressive breast cancer cell lines when compared with less aggressive cell lines. However, the lower levels in the aggressive lines were inducible by interferon‐γ (IFN‐γ). Because Nmi has been reported to be a transcription cofactor that augments IFN‐γ induced transcription activity, we decided to test whether Nmi regulates expression of Dkk1, which is also inducible by IFN‐γ. We established stable clones constitutively expressing Nmi in MDA‐MB‐231 (breast) and MDA‐MB‐435 (melanoma) cell lines. Dkk1 was significantly up‐regulated in the Nmi expressing clones concurrent with reduced levels of the critical transcription cofactor of Wnt pathway, β‐catenin. Treatment of the Nmi expressors with blocking antibody to Dkk1 restored β‐catenin protein levels. c‐Myc is a known downstream target of activated β‐catenin signaling. Treatment of Nmi expressors with the proteosome inhibitor MG132, resulted in elevated β‐catenin levels with concomitant elevation of c‐Myc levels. Our functional studies showed that constitutive expression of Nmi reduced the ability of tumor cells for the invasion, anchorage independent growth and tumor growth in vivo. Collectively, the data suggest that overexpression of Nmi inhibits the Wnt/β‐catenin signaling via up‐regulation of Dkk1 and retards tumor growth. © 2009 UICC
Proteomic and phosphoproteomic alterations in benign, premalignant and tumor human breast epithelial cells and xenograft lesions: Biomarkers of progression
Authors: Kim So Hee , Miller Fred R. , Tait Larry , Zheng Jie , Novak Raymond F. 
Published: January 2009

AbstractThe MCF10A human breast epithelial cell lineage includes the benign MCF10A cells, premalignant cells (MCF10AT, MCF10ATG3B) and malignant MCF10CA1a tumor cells. The premalignant and tumor cells recapitulate the progressive alterations associated with the temporal development of PBD and carcinoma. Ras protein levels were elevated by 6.9‐, 22.4‐ and 32.2‐fold in 10AT, 10ATG3B and 10CA1a cells, respectively, relative to 10A cells. K‐Ras was not detected, N‐Ras levels were unchanged; Rac and Rho levels increased in 10CA1a tumor cells. Phospho‐phosphatidylinositol 3‐kinase, phosphoinositide‐dependent protein kinase 1 (PDK1), phospho‐PDK1, phospho‐eukaryotic translation initiation factor 4E (eIF4E) and phospho‐eukaryotic initiation factor 4E binding protein 1 (4E‐BP1) levels progressively increased in the cell lineage, with the greatest increase monitored in 10CA1a tumor cells. Phospho Ser 473 and Thr 408 Akt levels increased 10.2‐ and 136‐fold in 10CA1a cells, respectively, relative to 10A cells. Phospho‐p70S6 kinase (p70S6K) increased >2‐fold in 10CA1a cells, relative to 10A cells. Immunohistochemistry confirmed Ras, phospho‐Akt and phospho‐p70S6K (Thr 421/ Ser 424) expression in lesions arising from premalignant and tumor cells. FOXO 1, phospho‐FOXO 1 and phospho‐FOXO 4 were significantly elevated in 10ATG3B premalignant and 10CA1a tumor cells. Phospho‐FOXO 3a was progressively elevated, with the greatest levels detected in 10CA1a tumor cells. Immunohistochemistry revealed that phospho‐FOXO 1, 3a and 4 staining was less in benign lesions, but elevated in advanced 10ATG3B and malignant 10CA1a lesions, showing a correspondence between the cells and lesions. Hence, phospho‐Akt and phospho‐FOXO 1, 3a and 4 merit consideration as biomarkers of tumorigenic risk from hyperplastic breast tissue. © 2009 UICC
PTD4‐apoptin protein therapy inhibits tumor growth in vivo
Authors: Sun Jun , Yan Ying , Wang Xiao‐Ting , Liu Xiao‐Wen , Peng Dong‐Jun , Wang Min , Tian Jun , Zong Yi‐Qiang , Zhang Ying‐Hui , Noteborn Mathieu H.M. , Qu Shen 
Published: January 2009

AbstractApoptin protein harbors tumor‐selective cell death activity, which makes it a potential anticancer therapy candidate. This study reports an apoptin therapy approach based on protein transduction domain 4 (PTD4)‐mediated transduction of recombinant apoptin protein. In vitro, the PTD4‐apoptin fusion protein is located in the nucleus and induces cell death in, e.g., human hepatocarcinoma HepG2 cells. In normal human L‐02 hepatocytes, PTD4‐apoptin protein retained mainly cytoplasmic and did not induce detectable levels of cell death, illustrating that the PTD4 domain does not affect apoptin's tumor‐selective characteristics. In vivo, liver, cervix and gastric carcinoma xenografts treated with PTD4‐apoptin protein for 6 days via the tumor epidermis exhibited a significant tumor growth inhibition because of apoptin‐mediated cell death. In addition, treatment of human hepatocarcinoma xenografts during 3 weeks showed that PTD4‐apoptin protein has significant anticancer activity, whereas control treatment with PTD4‐enhanced green fluorescence protein or saline did not. Cell death and disruption of the tumor integrity were apparent in the PTD4‐apoptin transduced xenografted tumors. As important, although PTD4‐apoptin protein could be detected in the epidermal tissue covering the subcutaneous tumor tissue and in several organs, such as liver and brain, of the treated mice, no tissue disruption or signs of cell death could be detected. Our in vivo data reveal that apoptin protein delivery constitutes a novel powerful and safe anticancer therapy. © 2009 UICC
ΔNp63α‐dependent expression of Id‐3 distinctively suppresses the invasiveness of human squamous cell carcinoma
Authors: Higashikawa Koichiro , Yoneda Shingo , Tobiume Kei , Saitoh Masao , Taki Masayuki , Mitani Yoshitsugu , Shigeishi Hideo , Ono Shigehiro , Kamata Nobuyuki 
Published: January 2009

Abstractp63 is a member of the p53 family and ΔNp63α is the dominant‐expressing isoform of p63 in basal layer of normal stratified epithelium and human squamous cell carcinoma (SCC) cells. We have previously reported that down‐regulation of p63 was accompanied with epithelial‐to‐mesenchymal transition (EMT) by Snail‐expressing SCC cells, in which re‐expression of ΔNp63α diminished their invasiveness (Higashikawa K, Yoneda S, Tobiume K, Taki M, Shigeishi H, Kamata N. Snail‐induced down‐regulation of ΔNp63α acquires invasive phenotype of human squamous cell carcinoma. Cancer Res 2007;67:9207–13). In this study, we found that ΔNp63α positively regulated inhibitor of differentiation‐3 (Id‐3) expression. Id is a dominant negative regulator of E2A which is a transcriptional repressor of E‐cadherin. Enforced expression of Id‐3 was incapable of invoking E‐cadherin expression in the SCC cells with EMT phenotype, whereas it significantly impaired their invasiveness with down‐regulation of matrix‐metalloproteinase‐2 (MMP‐2) expression. Reporter gene assay revealed that the Ets‐1‐induced MMP‐2 promoter activity was suppressed by the Id‐3, while the Id‐3‐dependent E‐cadherin promoter activity was remarkably reduced in the presence of Snail. Furthermore, knockdown of p63 in SCC cells significantly decreased Id‐3 expression, in which up‐regulation of MMP‐2 expression was concomitant with the acquired invasiveness. These findings propose a particular role of the off‐signaling of the ΔNp63α‐Id‐3 axis incident to Snail‐mediated EMT for the MMP‐2‐dependent invasiveness in SCC cells. © 2009 UICC
Ghrelin inhibits early osteogenic differentiation of C3H10T1/2 cells by suppressing Runx2 expression and enhancing PPARγ and C/EBPα expression
Authors: Kim Sang Wan , Choi Ok Kyung , Jung Ju Yeon , Yang Jae‐Yeon , Cho Sun Wook , Shin Chan Soo , Park Kyong Soo , Kim Seong Yeon 
Published: January 2009

AbstractGhrelin is a 28‐residue peptide identified in the stomach as an endogenous ligand of the growth hormone secretagogue receptor that is expressed in a variety of peripheral tissues, as well as in the brain. In previous studies, ghrelin has been shown to stimulate both adipogenic differentiation from preadipocytes and osteogenic differentiation from preosteoblasts or primary osteoblasts. This study was undertaken to investigate the direct effect of ghrelin on the lineage allocation of mesenchymal stem cells (MSCs). We identified ghrelin receptor mRNA in C3H10T1/2 cells, and we found the levels of this mRNA to be attenuated during osteogenic differentiation. Treatment of cells with ghrelin resulted in both proliferation and inhibition of caspase‐3 activity. In addition, ghrelin decreased serum deprivation‐induced bax protein expression and release of cytochrome c from the mitochondria, whereas it increased bcl‐2 protein expression. Moreover, ghrelin inhibited early osteogenic differentiation, as shown by alkaline phosphatase activity and staining, and inhibited osteoblast‐specific genes expression by altering Runx2, PPARγ, and C/EBPα protein expression. J. Cell. Biochem. 106: 626–632, 2009. © 2009 Wiley‐Liss, Inc.
The TRβ1 is essential in mediating T3 action on Akt pathway in human pancreatic insulinoma cells
Authors: Verga Falzacappa Cecilia , Patriarca Valentina , Bucci Barbara , Mangialardo Claudia , Michienzi Simona , Moriggi Giulia , Stigliano Antonio , Brunetti Ercole , Toscano Vincenzo , Misiti Silvia 
Published: January 2009

AbstractThyroid hormone action, widely recognized on cell proliferation and metabolism, has recently been related to the phosphoinositide 3 kinase (PI3K), an upstream regulator of the Akt kinase and the involvement of the thyroid hormone receptor β1 has been hypothesized. The serine‐threonine kinase Akt can regulate various substrates that drive cell mass proliferation and survival. Its action has also been characterized in pancreatic β‐cells. We previously demonstrated that Akt activity and its activation in the insulinoma cell line hCM could be considered a specific target of the non‐genomic action of T3. In this study we analyzed the molecular pathways involved in the regulation of cell proliferation, survival, size, and protein synthesis by T3 in a stable TRβ1 interfered insulinoma cell line, derived from the hCM, and evidenced a strong regulation of both physiological and molecular events by T3 mediated by the thyroid hormone receptor β1. We showed that the thyroid receptor β1 mediates the T3 regulation of the cdk4·cyc D1·p21CIP1·p27KIP1 complex formation and activity. In addition TRβ1 is essential for the T3 upregulation of the Akt targets β‐catenin, p70S6K, and for the phosphorylation of Bad and mTOR. We demonstrated that the β1 receptor mediates the T3 upregulation of protein synthesis and cell size, together with the cell proliferation and survival, playing a crucial role in the T3 regulation of the PI3K/Akt pathway. J. Cell. Biochem. 106: 835–848, 2009. © 2009 Wiley‐Liss, Inc.
Unusual sterolic mixture, and 24‐isopropylcholesterol, from the sponge Ciocalypta sp. reduce cholesterol uptake and basolateral secretion in Caco‐2 cells
Authors: Do Hong Quang , Van Landeghem Laurianne , Wielgosz‐Collin Gaëtane , Takoudju Martin , Huvelin Jean‐Michel , Kornprobst Jean‐Michel , Bard Jean‐Marie , Barnathan Gilles , Nazih Hassan 
Published: January 2009

AbstractAn unusual sterolic mixture (82.3% of 24‐isopropylated sterols) and its major component, 24‐isopropylcholesterol, isolated from a marine sponge, Ciocalypta sp. (Halichondriidae), reduce cholesterol uptake, basolateral secretion and ACAT‐2 mRNA expression and increase the expression of ABCA1 mRNA in Caco‐2 cells. The decreases of cholesterol uptake and secretion induced by 24‐isopropylcholesterol alone were more than that of both the sterolic mixture and β‐sitosterol. These data add a new sterol, 24‐isopropylcholesterol, to sterols that may reduce intestinal cholesterol absorption. J. Cell. Biochem. 106: 659–665, 2009. © 2009 Wiley‐Liss, Inc.
The autonomous notch signal pathway is activated by baicalin and baicalein but is suppressed by niclosamide in K562 cells
Authors: Wang An‐Ming , Ku Hung‐Hai , Liang Yu‐Chih , Chen Yen‐Chou , Hwu Yuh‐Ming , Yeh Tien‐Shun 
Published: January 2009

AbstractThe Notch signaling pathway plays important roles in a variety of cellular processes. Aberrant transduction of Notch signaling contributes to many diseases and cancers in humans. The Notch receptor intracellular domain, the activated form of Notch receptor, is extremely difficult to detect in normal cells. However, it can activate signaling at very low protein concentration to elicit its biological effects. In the present study, a cell based luciferase reporter gene assay was established in K562 cells to screen drugs which could modulate the endogenous CBF1‐dependent Notch signal pathway. Using this system, we found that the luciferase activity of CBF1‐dependent reporter gene was activated by baicalin and baicalein but suppressed by niclosamide in both dose‐ and time‐dependent manners. Treatment with these drugs modulated endogenous Notch signaling and affected mRNA expression levels of Notch1 receptor and Notch target genes in K562 cells. Additionally, erythroid differentiation of K562 cells was suppressed by baicalin and baicalein yet was promoted by niclosamide. Colony‐forming ability in soft agar was decreased after treatment with baicalin and baicalein, but was not affected in the presence of niclosamide. Thus, modulation of Notch signaling after treatment with any of these three drugs may affect tumorigenesis of K562 cells suggesting that these drugs may have therapeutic potential for those tumors associated with Notch signaling. Taken together, this system could be beneficial for screening of drugs with potential to treat Notch signal pathway‐associated diseases. J. Cell. Biochem. 106: 682–692, 2009. © 2009 Wiley‐Liss, Inc.
Correct identification of oxidized histidine residues using electron‐transfer dissociation
Authors: Srikanth Rapole , Wilson Jonathan , Vachet Richard W. 
Published: January 2009

AbstractOxidative modification to the side chain of histidine can noticeably change the collision‐induced dissociation (CID) pathways of peptides containing this oxidized residue. In cases where an oxidized peptide consists two or more isomers differing only in the site of modification, oxidation to histidine usually causes the other oxidized sites to be mis‐assigned in CID spectra. These spectral misassignments can sometimes be avoided by using multiple stages of MS/MS (MSn) or via specially optimized liquid chromatographic separation conditions. In this manuscript, we demonstrate that these misassignments can be more readily and easily avoided by using electron‐transfer dissociation (ETD) to dissociate the oxidized peptides. Furthermore, we find that the relative insensitivity of ETD to side‐chain chemistry allows the extent of oxidative modification to be determined readily for peptide isomers having more than one site of oxidation. The current results along with previous studies of oxidized peptides suggest that ETD is probably a better technique than CID for obtaining correct sequence and modification information for oxidized peptides. Copyright © 2009 John Wiley & Sons, Ltd.