bluuebunny/crossref_metadata_2025_split huggingface dataset:
The increased expression of receptor activator of nuclear‐κB ligand (RANKL) of multiple myeloma bone marrow stromal cells is inhibited by the bisphosphonate ibandronate
Authors: Fernández Mireya , Pino Ana M , Figueroa Paula , Rodríguez Juan P 
Published: May 2010

AbstractThe receptor activator of nuclear factor‐kappaB ligand (RANKL) and interleukin‐1beta are osteoclast activating factors which are abnormally expressed in bone marrow stromal cells and plasma cells of multiple myeloma patients. In this work we analyzed RANKL expression in human bone marrow mesenchymal stromal cells and the effect of the bisphosphonate ibandronate on RANKL expression after IL‐1beta activation of ERK pathway. Mesenchymal stromal cells were obtained from bone marrow iliac aspirates from multiple myeloma patients at stages II/III and non‐osteoporotics control donors; these cells were maintained under long‐term culture conditions. Cells were cultured in the presence or the absence of 5 ng/ml IL‐1beta and/or 5 µM ibandronate, during selected periods. mRNA for RANKL and protein levels were assayed by RT‐PCR and Western blot, respectively. Human bone marrow stromal cell line HS‐5 was used for assessing IL 1beta‐ and ibandronate‐ERK phosphorylation responses. Multiple myeloma mesenchymal stromal cells differentiate from control cells by increased basal RANKL expression. IL‐1beta up regulated RANKL expression showed dependent on activated MEK/ERK pathway. Finally, the bisphosphonate ibandronate, that hindered activation of the MEK/ERK pathway significantly inhibited both basal and IL‐1beta dependent RANKL expression by cells. Results indicate that RANKL expression involves the MEK/ERK pathway in multiple myeloma mesenchymal stromal cells, and that early obstruction of this path, such as that achieved with ibandronate, significantly deters RANKL protein expression. J. Cell. Biochem. 111: 130–137, 2010. © 2010 Wiley‐Liss, Inc.
Roles of GRP78 in physiology and cancer
Authors: Zhang Lu‐Hua , Zhang Xiang 
Published: May 2010

AbstractAs one member of 70 kDa heat shock proteins, glucose‐regulated protein 78 (GRP78) participates in protein folding, transportation and degradation. This sort of capacity can be enhanced by stresses under which GRP78 is induced rapidly. Unlike its homologues, GRP78 presents multifaceted subcellular position: When ER retention, it serves as the switch of unfolded protein response; When mitochondrial binding, it directly interacts with apoptotic executors; When cell surface residing, it recognizes extracellular ligands, transducing proliferative signals, especially in certain tumors. The close correlation between GRP78 and neoplasm provides us further insight into the event of carcinogenesis and cancer cell chemoresistance, indicating its prognostic predicting significance and validating potential therapeutics for clinical usage, especially because its small molecular inhibitors are emerging quickly these years. What's more, GRP78‐related signaling may be helpful for clearer understanding of its biological mechanisms. J. Cell. Biochem. 110: 1299–1305, 2010. © 2010 Wiley‐Liss, Inc.
Taiwan cobra phospholipase A2 elicits posttranscriptional up‐regulation of ADAM17 in human neuroblastoma SK‐N‐SH cells
Authors: Liu Wen‐Hsin , Chen Ku‐Chung , Chiou Yi‐Ling , Lin Shinne‐Ren , Chang Long‐Sen 
Published: May 2010

AbstractTaiwan cobra phospholipase A2 (PLA2) treatment promoted proADAM17 processing into mature ADAM17 in human neuroblastoma SK‐N‐SH cells. The abolishment of catalytic activity caused a drastic drop in the PLA2 ability to induce ADAM17 maturation, and lysophosphatidylcholine treatment mimicked the effect of PLA2. ADAM17 activity measurement, ADAM17 cell surface levels, TNFR2 ectodomain shedding, and ADAM17 mRNA transcription supported that posttranscriptional up‐regulation of ADAM17 occurred in PLA2‐treated SK‐N‐SH cells. PLA2 treatment induced p38 MAPK activation and ERK inactivation. p38 MAPK activation suppression by SB202190 (p38 MAPK inhibitor) abolished posttranscriptional up‐regulation of ADAM17 in PLA2‐treated cells, while treatment with U0126 (MEK1 and MEK2 inhibitor) increased ADAM17 maturation in SK‐N‐SH cells. Constitutively active MEK1 expression abrogated PLA2‐induced ADAM17 maturation. Taken together, our data indicate that PLA2‐evoked p38 MAPK activation and ERK inactivation are involved in ADAM17 posttranscriptional up‐regulation, and suggest that the action of PLA2 is catalytic activity‐dependent. J. Cell. Biochem. 111: 148–157, 2010. © 2010 Wiley‐Liss, Inc.
Transcriptional and post‐transcriptional control of DNA methyltransferase 3B is regulated by phosphatidylinositol 3 kinase/Akt pathway in human hepatocellular carcinoma cell lines
Authors: Mei Chuanzhong , Sun Lidong , Liu Yonglei , Yang Yong , Cai Xiumei , Liu Mingzhu , Yao Wantong , Wang Can , Li Xin , Wang Liying , Li Zengxia , Shi Yinghong , Qiu Shuangjian , Fan Jia , Zha Xiliang 
Published: May 2010

AbstractDNA methyltransferases (DNMTs) are essential for maintenance of aberrant methylation in cancer cells and play important roles in the development of cancers. Unregulated activation of PI3K/Akt pathway is a prominent feature of many human cancers including human hepatocellular carcinoma (HCC). In present study, we found that DNMT3B mRNA and protein levels were decreased in a dose‐ and time‐dependent manner in HCC cell lines with LY294002 treatment. However, we detected that LY294002 treatment did not induce increase of the degradation of DNMT3B protein using protein decay assay. Moreover we found that Akt induced alteration of the expression of DNMT3B in cells transfected with myristylated variants of Akt2 or cells transfected with small interfering RNA respectively. Based on DNMT3B promoter dual‐luciferase reporter assay, we found PI3K pathway regulates DNMT3B expression at transcriptional level. And DNMT3B mRNA decay analysis suggested that down‐regulation of DNMT3B by LY294002 is also post‐transcriptional control. Furthermore, we demonstrated that LY294002 down‐regulated HuR expression in a time‐dependent manner in BEL‐7404. In summary, we have, for the first time, demonstrate that PI3K/Akt pathway regulates the expression of DNMT3B at transcriptional and post‐transcriptional levels, which is particularly important to understand the effects of PI3K/Akt and DNMT3B on hepatocarcinogenesis. J. Cell. Biochem. 111: 158–167, 2010. © 2010 Wiley‐Liss, Inc.
UV light killing efficacy of fluorescent protein‐expressing cancer cells in vitro and in vivo
Authors: Kimura Hiroaki , Lee Claudia , Hayashi Katsuhiro , Yamauchi Kensuke , Yamamoto Norio , Tsuchiya Hiroyuki , Tomita Katsuro , Bouvet Michael , Hoffman Robert M. 
Published: May 2010

AbstractWe investigated the cell‐killing efficacy of UV light on cancer cells expressing GFP in the nucleus and RFP in the cytoplasm (dual‐color cells). After exposure to various doses of UVA, UVB, or UVC, apoptotic and viable cells were quantitated under fluorescence microscopy using dual‐color 143B human osteosarcoma cells, HT‐1080 human fibrosarcoma cells, Lewis lung carcinoma (LLC), and XPA‐1 human pancreatic cancer cells in vitro. UV‐induced cancer cell death was wave‐length and dose dependent, as well as cell‐line dependent. After UVA exposure, most cells were viable even when the UV dose was increased up to 200 J/m2. With UVB irradiation, cell death was observed with irradiation at 50 J/m2. For UVC, as little as 25 J/m2 UVC irradiation killed approximately 70% of the 143B dual‐color cells. This dose of UVB or UVA had almost no effect on the cancer cells. UV‐induced cancer cell death varied among the cell lines. Cell death began about 4 h after irradiation and continued until 10 h after irradiation. UVC exposure also suppressed cancer cell growth in nude mice in a model of minimal residual cancer (MRC). No apparent side effects of UVC exposure were observed. This study opens up the possibility of UVC treatment for MRC after surgical resection. J. Cell. Biochem. 110: 1439–1446, 2010. © 2010 Wiley‐Liss, Inc.
2,3,7,8‐Tetrachlorodibenzo‐p‐dioxin modifies expression and nuclear/cytosolic localization of bovine herpesvirus 1 immediate‐early protein (bICP0) during infection
Authors: Fiorito Filomena , Marfè Gabriella , Granato Giovanna E. , Ciarcia Roberto , De Blasio Emma , Tafani Marco , Florio Salvatore , De Martino Luisa , Muzi Gianmarco , Pagnini Ugo , Giordano Antonio 
Published: May 2010

AbstractOur previous studies have demonstrated that 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) increases Bovine Herpesvirus 1 (BHV‐1) replication through a dose‐dependent increase in cytopathy and increased viral titer. Furthermore, TCDD was able to trigger BHV‐1‐induced apoptosis by up‐regulating the activation of initiator caspases 8 and 9, as well as of effector caspase 3. Since TCDD activates caspase 3 after 4 h of infection, we have hypothesized an involvement of BHV‐1 infected cell protein 0 (bICP0) in this process. Such protein, the major transcriptional regulatory protein of BHV‐1, has been shown to indirectly induce caspase 3 activation and apoptosis. In order to elucidate the role of bICP0 in this apoptotic pathway, here we have analyzed the effects of TCDD on bICP0 expression. Following infection of bovine cells with BHV‐1, we detected apoptotic features already at 12 h after infection, only in TCDD exposed groups. Furthermore, in the presence of different doses of TCDD, we observed a time‐dependent modulation and increase of bICP0 gene expression levels, as revealed by RT‐PCR analysis. Western blot analysis and immunocytochemistry revealed that TCDD induced an increase of bICP0 protein levels in a dose‐dependent manner, compared to unexposed groups. Moreover, Western blot analysis of nuclear and cytosolic fractions of infected cells revealed that TCDD anticipated the presence of bICP0 protein in the cytoplasm. In conclusion, both the increase of replication of BHV‐1 and anticipation of BHV‐1‐induced apoptosis could be the result of a relationship between TCDD and bICP0. J. Cell. Biochem. 111: 333–342, 2010. © 2010 Wiley‐Liss, Inc.
Decreased expression of insulin‐like growth factor binding protein‐5 during N‐(4‐hydroxyphenyl)retinamide‐induced neuronal differentiation of ARPE‐19 human retinal pigment epithelial cells: Regulation by CCAAT/enhancer‐binding protein
Authors: Samuel William , Kutty R. Krishnan , Vijayasarathy Camasamudram , Pascual Iranzu , Duncan Todd , Redmond T. Michael 
Published: May 2010

AbstractInsulin‐like growth factor (IGF)‐binding protein‐5 (IGFBP5), an important member of the IGF axis involved in regulating cell growth and differentiation, acts by modulating IGF signaling and also by IGF‐independent mechanisms. We identified IGFBP5 by microarray analysis as a gene differentially regulated during N‐(4‐hydroxyphenyl)retinamide (4HPR)‐induced neuronal differentiation of human retinal pigment epithelial (RPE) cells. IGFBP5 is expressed in human RPE cells, and its expression, mRNA as well as protein, is greatly decreased during the 4HPR‐induced neuronal differentiation. Exogenous IGFBP5 does not block the neuronal differentiation indicating that IGFBP5 down‐regulation may not be a prerequisite for the neuronal differentiation. IGFBP5 down‐regulation, similar to neuronal differentiation, is mediated by the MAPK pathway since U0126, an inhibitor of MEK1/2, effectively blocked it. The overexpression of transcription factor CCAAT/enhancer binding protein‐β (C/EBPβ) inhibited the 4HPR‐induced down‐regulation of IGFBP5 expression and the neuronal differentiation of RPE cells. Interestingly, the binding of C/EBPβ to the IGFBP5 promoter was decreased by the 4HPR treatment as indicated by gel shift and chromatin immunoprecipitation analyses. Further, the deletion of C/EBP response element from IGFBP5 promoter markedly decreased the basal promoter activity and abolished its responsiveness to 4HPR treatment in reporter assays, suggesting that the expression of IGFBP5 is regulated by C/EBP. Thus, our results clearly demonstrate that the IGFBP5 expression is down‐regulated during 4HPR‐induced neuronal differentiation of human RPE cells through a MAPK signal transduction pathway involving C/EBPβ. J. Cell. Physiol. 224: 827–836, 2010. Published 2010 Wiley‐Liss, Inc.
Divergent molecular mechanisms underlying the pleiotropic functions of macrophage inhibitory cytokine‐1 in cancer
Authors: Mimeault Murielle , Batra Surinder K. 
Published: May 2010

AbstractMultifunctional macrophage inhibitory cytokine‐1, MIC‐1, is a member of the transforming growth factor‐β (TGF‐β) superfamily that plays key roles in the prenatal development and regulation of the cellular responses to stress signals and inflammation and tissue repair after acute injuries in adult life. The stringent control of the MIC‐1 expression, secretion, and functions involves complex regulatory mechanisms and the interplay of other growth factor signaling networks that control the cell behavior. The deregulation of MIC‐1 expression and signaling pathways has been associated with diverse human diseases and cancer progression. The MIC‐1 expression levels substantially increase in cancer cells, serum, and/or cerebrospinal fluid during the progression of diverse human aggressive cancers, such as intracranial brain tumors, melanoma, and lung, gastrointestinal, pancreatic, colorectal, prostate, and breast epithelial cancers. Of clinical interest, an enhanced MIC‐1 expression has been positively correlated with poor prognosis and patient survival. Secreted MIC‐1 cytokine, like the TGF‐β prototypic member of the superfamily, may provide pleiotropic roles in the early and late stages of carcinogenesis. In particular, MIC‐1 may contribute to the proliferation, migration, invasion, metastases, and treatment resistance of cancer cells as well as tumor‐induced anorexia and weight loss in the late stages of cancer. Thus, secreted MIC‐1 cytokine constitutes a new potential biomarker and therapeutic target of great clinical interest for the development of novel diagnostic and prognostic methods and/or cancer treatment against numerous metastatic, recurrent, and lethal cancers. J. Cell. Physiol. 224: 626–635, 2010. © 2010 Wiley‐Liss, Inc.
Synthesis of imidazolin‐2‐ones by rearrangement of N‐carbamoyliminium salts derived from 4‐hydroxyimidazolidin‐2‐ones
Authors: Hough T. L. 
Published: May 2010

AbstractThe action of trifluoroacetic acid on 4‐hydroxyimidazolidin‐2‐ones 9a,b,c induces the formation of N‐carbamoyliminium salts 10a,b,c which rearrange to imidazolin‐2‐ones 11a,b,c. The reactions proceed in high yield at ambient temperatures.
Synthesis and spectral properties of 4‐(ortho‐R‐benzylideneamine)‐5‐[2‐(2‐pyridyl)ethenyl]‐3‐methylisoxazole
Authors: Eduardo Cortés C. , Eduardo Cortés R. , Martínez Roberto , Avila Gustavo , Sandoval Arturo 
Published: May 2010

AbstractThe preparation of several 5,4‐disubstituted 3‐methylisoxazoles is described. The structure of all products was corroborated by ir, 1H‐nmr and mass spectrometry.
Sels de n‐alcoxypyridinium porteurs d'une fonction cetone dans leur chaine alcoxyle: Synthese et reactivite vis‐à‐vis d'amines secondaires
Authors: Sliwa Henri , Randria‐Raharimanana Clarisse 
Published: May 2010

AbstractLa réaction de l' α‐bromo isobutyrophénone sur les N‐oxydes de pyridine, de γ‐ et de β‐picoline, en présence de nitrate d'argent, conduit à des sels de N‐alcoxy pyridinium et picolinium porteurs d'une fonction cétone dans leur chaĉne alcoxyle. Soumis à l'action de la pyrrolidine ces sels sont convertis en ω‐pyrrolidino butadiènyl‐4 isoxazolinols‐3 substitués ou non par un groupe méthyle dans leur chaĉne butadiénique. La réaction precède selon un mécanisme PARC‐ANRO (Proton Abstraction, Ring Closure — Addition of a Nucleophile, Ring Opening) comme le confirme l'isolement du sel d'isoxazolinopyridinium intermédiaire issu de la premiere phase de cette séquence. Cette conversion hétérocyclique, qui peut constituer une nouvelle approche de la synthése de dérives terpénoïdes, est concurrencée, dans le cas du sel dérivé du N‐oxyde de β‐picoline, par une nouvelle fragmentation alcoxylogue du mode A de la classification de Katritzky.
The syntheses of 5‐amino‐3‐t‐butylisothiazole and 3‐amino‐5‐t‐butylisothiazole
Authors: Hackler Ronald E. , Burow Kenneth W. , Kaster Sylvester V. , Wickiser David I. 
Published: May 2010

AbstractA general synthesis of 3‐amino‐3‐alkylpropenenitriles is described. These intermediates are further transformed to 5‐amino‐3‐alkylisothiazoles. Also described is the synthesis of the novel isomer, 3‐amino‐5‐t‐butyl‐isothiazole.
Benzotriazol‐1‐ylmethylammonium salts synthesis and reactivity
Authors: Katritzky Alan R. , Hughes Craig V. , Rachwal Stanislaw 
Published: May 2010

AbstractBenzotriazol‐1‐ylmethylamines on treatment with alkylating agents afford benzotriazol‐1‐ylmethylammoni‐um salts, also available from reactions of chloromethylbenzotriazole with tertiary amines. In deuterated solvents under basic conditions the methylene protons of these salts exchange with deuterium. At elevated temperatures, an alkyl group substituent migrated from the ammonium center to the benzotriazolyl N‐3. Reactions of the salts with Grignard reagents afforded various products arising from substitution of the ammonium moiety and/or from attack on the benzotriazolyl N‐3 or on the benzenoid ring.
A facile synthesis of 6‐alkoxy‐2,4‐diaryl‐5‐cyanopyridine
Authors: Al‐Arab Mohammad M. 
Published: May 2010

AbstractA new synthesis of substituted pyridine is reported. The base catalyzed reaction of substituted chalcones with malononitrile using sodium ethoxide in ethanol at room temperature afforded 2,4‐diaryl‐5‐cyano‐6‐ethoxypyridine. Similarly, 2,4‐diaryl‐5‐cyano‐6‐methoxypyridine have been prepared in presence of sodium methoxide in methanol as a catalyst.
A general method for the preparation of 2‐substituted‐4‐oxo‐3‐quinolinecarboxylic acids
Authors: Kiely John S. , Huang Suchin , Lesheski Lawrence E. 
Published: May 2010

AbstractA general method for preparing 2‐substituted‐4‐oxo‐3‐quinolinecarboxylic acids and 2‐substituted‐4‐oxo‐1,8‐naphthyridine‐3‐carboxylic acids as new analogs in the quinolone class of antiinfectives has been developed. The reaction of a Grignard reagent in the presence of copper(I) iodide with the 4‐oxo‐3‐quinolinecar‐boxylic acid esters and 4‐oxo‐1,8‐naphthyridine‐3‐carboxylic acid esters yields the desired 2‐substituent. Re‐introduction of the 2,3‐double bond is effected by phenylselenation of the 3‐position, oxidation to the selen‐oxide, and in situ syn‐elimisation. Depending on the degree of steric crowding between the 2‐substituent and the 3‐carboxylic acid group, hydrolysis of the ester to the carboxylic acid could be carried out under acidic or basic conditions.
Polycondensed nitrogen heterocycles. Part 22. Pyrrolo[3,4‐d]‐1,2,3‐triazines: A new ring system as potential antineoplastic agent
Authors: Dattolo Gaetano , Cirrincione Girolamo , Almerico Anna Maria , Aiello Enrico 
Published: May 2010

AbstractDiazotization of the 3‐aminopyrrole‐4‐carboxamides 6a,b under different conditions directly led to the new ring system pyrrolo[3,4‐d]‐1,2,3‐triazine in excellent yields through an intramolecular coupling reaction. In all the cases it was impossible to isolate the intermediate 3‐diazopyrroles.
Dimroth rearrangement of 5‐hydrazino‐1,2,3‐thiadiazoles
Authors: L'Abbé Gerrit , Vanderstede Els 
Published: May 2010

AbstractThe reversible isomerization of 5‐hydrazino‐1,2,3‐thiadiazoles and 1‐amino‐5‐mercapto‐1,2,3‐triazoles has been established for an ester function at the 4‐position (4a ⇌ 5a). Thus, 4a was isolated by reacting 3a with two equivalents of hydrazine, whereas 5a resulted when an excess of hydrazine was used. Acid treatment of 5a yielded 4a again, and its hydrazone 8 was obtained from 5a and benzaldehyde. Compound 5a was also converted into the derivatives 6a, 7, 9 and 10a‐c. The less reactive 5‐chloro‐1,2,3‐thiadiazoles 3b,c afforded the bis‐heterocycles 6b,c on heating with hydrazine.
Synthesis of 4‐hydroxy‐3‐methylene‐2,2,10‐trimethyl‐2,3‐dihydrofuro[3,2‐b]‐acridin‐5(10H)‐one, a new synthetic analog of noracronycine
Authors: Reisch Johannes , Kamal G. M. , Gunaherath B. 
Published: May 2010

AbstractA new tetracyclic acridinone, 4‐hydroxy‐3‐methylene‐2,2,10‐trimethyl‐2,3‐dihydrofuro[3,2‐b]acridin‐5(10H)‐one (1), has been synthesized. The linear orientation of the furan ring was confirmed by an nOe experiment.
2,6‐Dihydroxy‐4H‐pyridazino[3,4,5‐de]quinazoline: A new ring system
Authors: Combs Donald W. , Rampulla Marianne S. 
Published: May 2010

AbstractThe synthesis and spectral properties of 2,6‐dihydroxy‐4H‐pyridazino[3,4,5‐de]quinazoline 1 are described. This compound represents the first member of a new tetraazatricyclic ring system and exhibits biological activity.
10th international symposium on the synthesis and applications of isotopes and isotopically labelled compounds—synthesis of compounds labelled with long‐lived isotopes Session 1: Monday, June 15, 2009
Authors: Hesk David , Derdau Volker 
Published: May 2010

AbstractAbstract: This session outlined methods useful for the synthesis of intermediates labeled with carbon‐13, carbon‐14 or tritium. Additional papers described the utilization of carbon‐14 and tritium intermediates in the synthesis of labelled compounds for use in the development of pharmaceutical and agricultural agents. Copyright © 2010 John Wiley & Sons, Ltd.
10th international symposium on the synthesis and applications of isotopes and isotopically labelled compounds—WBA‐drug discovery and development Session 12, Tuesday, June 16, 2009
Authors: Whitby Brian , Solon Eric 
Published: May 2010

AbstractAbstract: A survey of QWBA, using current methodologies was given followed by a discussion of possible future advances in using this technique. Copyright © 2010 John Wiley & Sons, Ltd.
Detection of hazelnut oil in extra‐virgin olive oil by analysis of polar components by micro‐solid phase extraction based on hydrophilic liquid chromatography and MALDI‐ToF mass spectrometry
Authors: Calvano Cosima D. , Aresta Antonella , Zambonin Carlo G. 
Published: May 2010

AbstractThe oil polar fraction may have a great potential for the characterization of vegetable oils and for the individuation of adulterations. In particular, adulteration of extra‐virgin olive oil (EVOO) with hazelnut oil (HO) is one of the most difficult ones to detect due to the similar composition as regards triacylglycerol, total sterol and fatty acid profile. A new micro‐solid phase extraction (µ‐SPE) procedure based on hydrophilic liquid chromatography (HILIC) micro‐columns was developed for the selective extraction and enrichment of polar compounds from EVOO and HO before matrix‐assisted laser desorption ionization time‐of‐flight mass spectrometry (MALDI‐ToF‐MS) analysis. The method permits a simple and fast qualitative analysis of the polar fraction of the oils under study; furthermore, some peaks (such as the m/z ions 496.39, 520.46 and 522.47) were found to be present only in HO, indicating that they could be diagnostic for the presence of HO in EVOO. In order to verify the potential of the method for the individuation of this adulteration, EVOO was progressively adulterated with variable quantities of HO, subjected to the HILIC enrichment and finally to MALDI‐ToF‐MS analysis; the detection of adulteration was possible up to the level of 5%. Eventually, diagnostic polar compounds were identified as lysophosphatidylcholine (LPC) (16 : 0/0 : 0), LPC (18 : 2/0 : 0), LPC (18 : 1/0 : 0) by means of capillary liquid chromatography‐electrospray ionization‐quadrupole‐ToF‐MS (CapLC‐ESI‐Q‐ToF‐MS) analysis. Copyright © 2010 John Wiley & Sons, Ltd.