bluuebunny/crossref_metadata_2025_split huggingface dataset:
Peroxotungstates and Their Citrate and Tartrate Derivatives
Authors: Hou Shu‐Ya , Zhou Zhao‐Hui , Lin Tao‐Ran , Wan Hui‐Lin 
Published: February 2006

AbstractThe reaction of potassium tungstate with the biologically relevant ligands citric and tartaric acid, in the presence of hydrogen peroxide, was investigated to discover the effect of pH variation on the product pattern. The reaction with citric acid led to the formation of the dimer K5[WO(O2)2(Hcit)H(Hcit)(O2)2OW]·6H2O (1; H4cit = citric acid) due to carboxyl‐carboxylic acid hydrogen bonding in the pH range 2–5; this complex can also be obtained by an exchange reaction between the oxo ligands of the dimeric hydrogencitrate tungstate K4[W2O5(Hcit)2]·4H2O (6) and H2O2. Interestingly, a novel dimeric peroxotungstate K3[W2O3(O2)4(OH)]·H2O (2), without the coordination of citrate ligands, was isolated in the pH range 7–9, as confirmed by 17O NMR solution studies. The reaction of potassium tungstate with (R,R)‐tartaric acid afforded the tartratoperoxotungstate K4[W2O2(O2)4{(R,R)‐tart}]·3H2O [3; H4tart = (R,R)‐tartaric acid] in the pH range 1–3. The dimeric peroxotungstate K2[W2O3(O2)4(H2O)2]·2H2O (4) was found to react with citric or tartaric acid at pH 2–5 or 2–3, respectively, to give species 1 and 3. Evidence that 1 exists as a dimer in solution is presented. The three complexes were characterized by elemental analysis, IR and NMR spectroscopy, and X‐ray structural analyses. The formation of these complexes is dictated by pH, and the thermal stabilities of 1 and 3 vary with the coordinated ligands. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Aminoethyl‐Functionalized Cyclopentadienyliridium Complexes: Photochemical C–H Activation and Carbonylation of Cycloalkanes
Authors: Chan Pek Ke , Leong Weng Kee , Krummel Karl I. , Garland Marc V. 
Published: February 2006

AbstractThe photochemical C–H activation of cycloalkanes by aminoethyl‐functionalized cyclopentadienyliridium complexes proceeds in a broadly similar way to that for their unfunctionalized analogues. In a carbon monoxide atmosphere, there is evidence that carbonylation to form the carboxaldehyde occurred with both systems. In situ infrared spectroscopic studies on these reactions allow the identification of several species present in low concentrations in the reaction mixture. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Facile and Reliable Synthesis of Tetraphenoxyborates and Their Properties
Authors: Malkowsky Itamar M. , Fröhlich Roland , Griesbach Ulrich , Pütter Hermann , Waldvogel Siegfried R. 
Published: February 2006

AbstractTetraphenoxyborates are reliably prepared in a two‐step sequence, exploiting less corrosive reagents like boric acid and the corresponding phenols. The broad scope of this transformation is demonstrated in 22 examples. Several solid‐state structures reveal the preferential conformation of the phenoxy moieties allowing cation interaction. Furthermore, a novel architecture of a phenoxy‐substituted tetraborate was found. Surprisingly, the tetraphenoxyborates exhibit a good stability in neutral and basic media. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
A basic study on humidity recovery using micro‐porous media: General characteristics and effect of material properties on transport performance
Authors: Wang Shixue , Utaka Yoshio , Tasaki Yutaka 
Published: February 2006

AbstractAs a first step toward evaluating factors that influence humidity and heat transfer from moist air to dry air through porous media having very small pores, the present paper attempts to clarify factors that influence moisture transport between constant‐temperature water and dry air through a porous media plate. The effect of the pore diameter of the porous plate on the humidity transport through a porous plate was found to depend strongly on the thickness and pore diameter of the porous plate. That is, the smaller the pore diameter and the thicker the plate, the greater the effect of the pore diameter on the humidity transfer. In addition, the performance of heat and mass transfer were confirmed to increase with respect to the increase of air velocity. In addition, a parameter called the humidity absorption rate was introduced to evaluate the utilization degree of the air capacity to absorb humidity. The humidity absorption rate decreased with increases in both air velocity and plate thickness. © 2006 Wiley Periodicals, Inc. Heat Trans Asian Res, 35(2): 137–151, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/htj.20102
Study on the chimney effect in natural air‐cooled electronic equipment casings under inclination: Proposal of a thermal design correlation that includes the porosity coefficient of an outlet opening
Authors: Kitamura Yoji , Ishizuka Masaru , Nakagawa Shinji 
Published: February 2006

AbstractNatural air‐cooling technologies for electronic equipment have the important advantages of no fan and high reliability. However, natural air cooling has lower cooling capability than fan air cooling, so enhancement of its cooling capability is required. This paper presents the results for experimental casings designed to employ the chimney effect in natural air‐cooled electronic equipment. The system casing is inclined to enhance the effectiveness of natural air cooling. Experiments were carried out using a thin laptop PC. We investigated the effect on cooling capability produced by inclining the casing and by varying the outlet positions and numbers and the porosity coefficient of the outlet openings. The results show that the temperatures inside the casing and heater surfaces are slightly diminished by the effect of increased inclination and porosity coefficient of outlet openings. Moreover, the increase in natural circulation flux in the casing was quantitatively proven by experiments. In addition, the experimental data were reduced to a Nusselt number–Rayleigh number correlation, $Nu_{\beta}^{\ast}=0.432Ra_{\beta}^{\ast0.322}$, by using a modified reference length. © 2006 Wiley Periodicals, Inc. Heat Trans Asian Res, 35(2): 122–136, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/htj.20103
The mathematical model of solidification latent heat under high cooling rate
Authors: Shan Yao , Xuena Gong , Lixin Dai , Chunying Ma , Junze Jin , Abudula Abuliti 
Published: February 2006

AbstractTreatment of solidification latent heat is a key point in solidification simulation by the finite difference method. When latent heat is dealt with in a traditional method of equivalent latent heat, it was found that heat was increased when casting with a high cooling rate, and then the simulation result was distorted. In this paper, a new method is proposed to deal with solidification latent heat. Moreover, a mathematical model was suggested, in which the latent heat can be dealt with accurately under high or normal cooling rates. By contrasting the simulation results from this new method with the traditional one, it was indicated that this new model can obtain more accurate simulation results than the traditional model under high or normal cooling rates. © 2006 Wiley Periodicals, Inc. Heat Trans Asian Res, 35(2): 115–121, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/htj.20104
Study on constant stress: Accelerated life tests of fouling thermal resistance
Authors: Shan‐rang Yang , Ling‐fang Sun , Feng Guo , Zhi‐ming Xu , Sheng‐ping Wang 
Published: February 2006

AbstractTo shorten the time of fouling tests, fouling life was defined. The statistical analysis method for type II‐censored exponential life data under constant‐stress accelerated life testing models and the accelerated coefficients a and b were obtained. By using an accelerated model, the estimators of the fouling life under usual stress could be obtained. A computing example was given. Results indicated that it is credible and feasible to perform accelerated life tests of asymptotic fouling thermal resistance, and will be of important value to experimental research of fouling. © 2006 Wiley Periodicals, Inc. Heat Trans Asian Res, 35(2): 110–114, 2006; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/htj.20105
The effect of operating parameters on water transport in PEM fuel cells
Authors: Hong Sun , Liejin Guo , Hongtan Liu 
Published: February 2006

AbstractWater content in the membrane and the presence of liquid water in the catalyst layers (CL) and the gas diffusion layers (GDL) play a very important role in the performance of a PEM fuel cell. To study water transport in a PEM fuel cell, a two‐phase flow mathematical model is developed. This model couples the continuity equation, momentum conservative equation, species conservative equation, and water transport equation in the membrane. The modeling results of fuel cell performances agree well with measured experimental results. Then this model is used to simulate water transport and current density distribution in the cathode of a PEM fuel cell. The effects of operating pressure, cell temperature, and humidification temperatures on the net water transfer through the membrane, liquid water saturation, and current density distribution are studied. © 2006 Wiley Periodicals, Inc. Heat Trans Asian Res, 35(2): 89–100, 2006; Published online in Wiley InterScience (www.interscience. wiley.com). DOI 10.1002/htj.20107
Comparative gene expression profiling reveals partially overlapping but distinct genomic actions of different antiestrogens in human breast cancer cells
Authors: Scafoglio Claudio , Ambrosino Concetta , Cicatiello Luigi , Altucci Lucia , Ardovino Mario , Bontempo Paola , Medici Nicola , Molinari Anna Maria , Nebbioso Angela , Facchiano Angelo , Calogero Raffaele A. , Elkon Ran , Menini Nadia , Ponzone Riccardo , Biglia Nicoletta , Sismondi Piero , Bortoli Michele De , Weisz Alessandro 
Published: March 2006

AbstractAntiestrogens used for breast cancer (BC) treatment differ among each other for the ability to affect estrogen receptor (ER) activity and thereby inhibit hormone‐responsive cell functions and viability. We used high‐density cDNA microarrays for a comprehensive definition of the gene pathways affected by 17β‐estradiol (E2), ICI 182,780 (ICI), 4OH‐tamoxifen (Tamoxifen), and raloxifene (RAL) in ER‐positive ZR‐75.1 cells, a suitable model to investigate estrogen and antiestrogen actions in hormone‐responsive BC. The expression of 601 genes was significantly affected by E2 in these cells; in silico analysis reveals that 86 among them include one or more potential ER binding site within or near the promoter and that the binding site signatures for E2F‐1, NF‐Y, and NRF‐1 transcription factors are significantly enriched in the promoters of genes induced by estrogen treatment, while those for CAC‐binding protein and LF‐A1 in those repressed by the hormone, pointing to novel transcriptional effectors of secondary responses to estrogen in BC cells. Interestingly, expression of 176 E2‐regulated mRNAs was unaffected by any of the antiestrogens tested, despite the fact that under the same conditions the transcriptional and cell cycle stimulatory activities of ER were inhibited. On the other hand, of 373 antiestrogen‐responsive genes identified here, 52 were unresponsive to estrogen and 25% responded specifically to only one of the compounds tested, revealing non‐overlapping and clearly distinguishable effects of the different antiestrogens in BC cells. As some of these differences reflect specificities of the mechanism of action of the antiestrogens tested, we propose to exploit this gene set for characterization of novel hormonal antagonists and selective estrogen receptor modulators (SERMs) and as a tool for testing new associations of antiestrogens, more effective against BC. J. Cell. Biochem. 98: 1163–1184, 2006. © 2006 Wiley‐Liss, Inc.
β‐cryptoxanthin stimulates apoptotic cell death and suppresses cell function in osteoclastic cells: Change in their related gene expression
Authors: Uchiyama Satoshi , Yamaguchi Masayoshi 
Published: March 2006

AbstractThe effect of β‐cryptoxanthin, a kind of carotenoid, on osteoclastic cells in mouse marrow culture system in vitro was investigated. The macrophage colony‐stimulating factor (M‐CSF)‐dependent bone marrow macrophages were cultured in the presence of M‐CSF (10 ng/ml) and receptor activator of NF‐κB ligand (RANKL; 25 ng/ml) for 4 days. The osteoclastic cells formed were further cultured in medium containing either vehicle or β‐cryptoxanthin (10−8–10−6 M) with or without M‐CSF (10 ng/ml) and RANKL (50 ng/ml) for 24–72 h. Osteoclastic cells were significantly decreased with culture of β‐cryptoxanthin (10−7 or 10−6 M) with or without M‐CSF and RANKL for 24, 48, or 72 h. β‐Cryptoxanthin (10−8 M)‐induced decrease in osteoclastic cells were significantly inhibited in the presence of caspase‐3 inhibitor (10−8 or 10−7 M). Agarose gel electrophoresis showed the presence of low‐molecular‐weight deoxyribonucleic acid (DNA) fragments of adherent cells cultured with β‐cryptoxanthin (10−7 or 10−6 M) for 24 or 48 h, indicating that the carotenoid induces apoptotic cell death. Apoptosis‐related gene expression was determined using reverse transcription‐polymerase chain reaction (RT‐PCR). Culture with β‐cryptoxanthin (10−7 or 10−6 M) for 24 or 48 h caused a significant increase in caspase‐3 mRNA expression in the presence or absence of M‐CSF and RANKL, while Bcl‐2 and Apaf‐2 mRNA expressions were significantly increased with culture of β‐cryptoxanthin (10−7 or 10−6 M) without M‐CSF and RANKL for 24 or 48 h. Akt‐1 mRNA expression was not significantly changed with culture of the carotenoid (10−7 or 10−6 M) for 24 or 48 h. Moreover, tartrate‐resistant acid phosphatase (TRACP) activity, or TRACP and cathepsin K mRNA expressions were significantly decreased with culture of β‐cryptoxanthin (10−6 M) in the presence or absence of M‐CSF and RANKL for 48 h. This study demonstrates that β‐cryptoxanthin has stimulatory effects on apoptotic cell death and suppressive effects on osteoclastic cell function. J. Cell. Biochem. 98: 1185–1195, 2006. © 2006 Wiley‐Liss, Inc.
Time sequence of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) and cisplatin treatment is responsible for a complex pattern of synergistic cytotoxicity
Authors: Kim Young‐Ho , Lee Yong J. 
Published: March 2006

AbstractThe combination of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) and cisplatin resulted in a greater cytotoxicity than could be accounted for by the addition of the cytotoxic effects of the agents alone. In this study, we hypothesized that the synergistic interaction between the two modalities can be changed when both the sequence and the time interval between the two treatments are varied. To test the hypothesis, human head‐and‐neck squamous‐cell carcinoma (HNSCC)‐6 cells were either pretreated with 0.01–0.5 µg/ml TRAIL for various times (0–24 h) followed by treatment with 5 µg/ml cisplatin or pretreated with 5 µg/ml cisplatin for various times (0–24 h) followed by treatment with 0.5 µg/ml TRAIL. In latter case, the synergistic effect was gradually increased when the time interval between the two treatments was increased. In former case, a maximal synergy occurred within 0–4 h of pretreatment with TRAIL. However, the synergistic effect was gradually decreased when the time interval between the two treatments was increased. Data from immunoblotting analysis reveal that a similar pattern emerged for the PARP cleavage and caspase activation. The synergistic effect is not associated with DR4, DR5, FADD, and FLIPL. Interestingly, a complex pattern of synergistic interaction between TRAIL and cisplatin is related to the cleavage of FLIPS. Although overexpression of FLIPS protected cells from FLIPS cleavage and apoptotic death, blockage of FLIPS cleavage by replacing Asp39 and Asp42 residues with alanine did not further enhance FLIPS‐mediated protection. Taken together, FLIPS cleavage reflects apoptotic damage, but it does not cause apoptosis. J. Cell. Biochem. 98: 1284–1295, 2006. © 2006 Wiley‐Liss, Inc.
Phosphatidylinositol 3‐kinase/Akt plays a role in sphingosine 1‐phosphate‐stimulated HSP27 induction in osteoblasts
Authors: Takai Shinji , Tokuda Haruhiko , Matsushima‐Nishiwaki Rie , Hanai Yoshiteru , Kato Kanefusa , Kozawa Osamu 
Published: March 2006

AbstractWe previously reported that p38 mitogen‐activated protein (MAP) kinase plays a part in sphingosine 1‐phosphate‐stimulated heat shock protein 27 (HSP27) induction in osteoblast‐like MC3T3‐E1 cells. In the present study, we investigated whether phosphatidylinositol 3‐kinase (PI3K)/protein kinase B (Akt) is involved in the induction of HSP27 in these cells. Sphingosine 1‐phosphate time dependently induced the phosphorylation of Akt. Akt inhibitor, 1L‐6‐hydroxymethyl‐chiro‐inositol 2‐(R)‐2‐O‐methyl‐3‐O‐octadecylcarbonate, reduced the HSP27 induction stimulated by sphingosine 1‐phosphate. The sphingosine 1‐phosphate‐induced phosphorylation of GSK‐3β was suppressed by Akt inhibitor. The sphingosine 1‐phosphate‐induced HSP27 levels were attenuated by LY294002 or wortmannin, PI3K inhibitors. Furthermore, LY294002 or Akt inhibitor did not affect the sphingosine 1‐phosphate‐induced phosphorylation of p38 MAP kinase and SB203580, a p38 MAP kinase inhibitor, had little effect on the phosphorylation of Akt. These results suggest that PI3K/Akt plays a part in the sphingosine 1‐phosphate‐stimulated induction of HSP27, maybe independently of p38 MAP kinase, in osteoblasts. J. Cell. Biochem. 98: 1249–1256, 2006. © 2006 Wiley‐Liss, Inc.
Synergistic regulation of endothelial tight junctions by antioxidant (Se) and polyunsaturated lipid (GLA) via Claudin‐5 modulation
Authors: Martin Tracey A. , Das Tapas , Mansel Robert E. , Jiang Wen G. 
Published: March 2006

AbstractTight junctions (TJs) in endothelial cells act as cell–cell adhesion structures, governing paracellular permeability (PCP). Disruption can lead to leaky vascular bed and potentially to oedema and swelling of tissues, the aetiology of mastalgia. These changes may also cause vascular spread of cancer cells. This study aimed to determine whether the function of TJs in endothelial cells can be strengthened by gamma linolenic acid (GLA), selenium (Se) and iodine (I) in the presence of 17beta‐estradiol (17β‐estradiol), which causes leakage of endothelial cells by disruption of TJs in endothelium. GLA, I, and Se individually increased transendothelial resistance. The combination of all three agents also had a significant effect on TER. Addition of GLA/Se/I reduced PCP of the endothelial cells. Treatment with GLA/Se/I reversed the effect of 17β‐estradiol in reducing TER and increasing PCP. Immunofluorescence revealed that after treatment with Se/I/GLA over 24 h there was increasing relocation to endothelial cell–cell junctions of the TJ proteins Claudin‐5, Occludin, and ZO‐1. Interestingly, this relocation was particularly evident with treatments containing I when probing with Claudin‐5 and those containing Se for Occludin. There was a small increase in overall protein levels when examined by Western blotting after treatment with GLA/Se/I when probed with Claudin‐5 and Occludin. We report that GLA, I, and Se alone, or in combination are able to strengthen the function of TJs in human endothelial cells, by way of regulating the distribution of Claudin‐5, Occludin, and ZO‐1. Interestingly, this combination was also able to completely reverse the effect of 17β‐estradiol in these cells. J. Cell. Biochem. 98: 1308–1319, 2006. © 2006 Wiley‐Liss, Inc.
Vitamin D3 suppresses the androgen‐stimulated growth of mouse mammary carcinoma SC‐3 cells by transcriptional repression of fibroblast growth factor 8
Authors: Kawata Hirotoshi , Kamiakito Tomoko , Takayashiki Norio , Tanaka Akira 
Published: February 2006

AbstractActive metabolites of vitamin A and D are well known to act as growth inhibitors in hormone‐related prostate and breast cancers. When various concentrations of 1α,25‐dihydroxyvitamin D3 (vitamin D3), all‐trans‐retinoic acid (ATRA) and 9‐cis retinoic acid (9‐cis RA) were examined, the androgen‐stimulated growth of mouse mammary carcinoma SC‐3 cells was inhibited by vitamin D3 alone in a dose‐dependent manner. A flow cytometer analysis showed that vitamin D3 leads SC‐3 cells to relative G1‐growth arrest after 72 h. Characterization of vitamin D3‐responsive genes using an oligonucleotide microarray demonstrated that 220 genes were upregulated at more than threefold, and 84 genes were downregulated to less than one‐third, compared with the testosterone‐stimulated SC‐3 cells. Neither cyclin‐dependent kinase inhibitors (CDKIs) nor the antiapoptotic bcl‐2 gene were induced in vitamin D3‐responsive genes, with the exception of a slight induction of p15INK4B. Importantly, fgf8 was markedly repressed in response to vitamin D3. The exogenous addition of FGF8 canceled the growth suppression by vitamin D3 in SC‐3 cells, suggesting that the repression of fgf8 is an indispensable step in vitamin D3‐mediated growth inhibition. In reporter assays using the ARE‐containing artificial construct and the natural androgen‐regulated PSA promoter, co‐transfection of the vitamin D receptor (VDR) and androgen receptor (AR) suppressed AR‐stimulated promoter activity. In addition, vitamin D3 also suppressed androgen‐stimulated promoter activity in the stably transfected SC‐3 cells. Moreover, VDR repressed the core promoter activity of fgf8 in COS1 cells and in the SC‐3 cells. All these findings strongly suggest that vitamin D3 serves as a negative regulator for both androgen‐related and fgf8 transcriptions. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Nuclease sensitive element binding protein 1 associates with the selenocysteine insertion sequence and functions in mammalian selenoprotein translation
Authors: Shen Qichang , Fan Lin , Newburger Peter E. 
Published: February 2006

AbstractBiosynthesis of selenium‐containing proteins requires insertion of the unusual amino acid selenocysteine by alternative translation of a UGA codon, which ordinarily serves as a stop codon. In eukaryotes, selenoprotein translation depends upon one or more selenocysteine insertion sequence (SECIS) elements located in the 3′‐untranslated region of the mRNA, as well as several SECIS‐binding proteins. Our laboratory has previously identified nuclease sensitive element binding protein 1 (NSEP1) as another SECIS‐binding protein, but evidence has been presented both for and against its role in SECIS binding in vivo and in selenoprotein translation. Our current studies sought to resolve this controversy, first by investigating whether NSEP1 interacts closely with SECIS elements within intact cells. After reversible in vivo cross‐linking and ribonucleoprotein immunoprecipitation, mRNAs encoding two glutathione peroxidase family members co‐precipitated with NSEP1 in both human and rat cell lines. Co‐immunoprecipitation of an epitope‐tagged GPX1 construct depended upon an intact SECIS element in its 3′‐untranslated region. To test the functional importance of this interaction on selenoprotein translation, we used small inhibitory RNAs to reduce the NSEP1 content of tissue culture cells and then examined the effect of that reduction on the activity of a SECIS‐dependent luciferase reporter gene for which expression depends upon readthrough of a UGA codon. Co‐transfection of small inhibitory RNAs directed against NSEP1 decreased its expression by approximately 50% and significantly reduced luciferase activity. These studies demonstrate that NSEP1 is an authentic SECIS binding protein that is structurally associated with the selenoprotein translation complex and functionally involved in the translation of selenoproteins in mammalian cells. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.