bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regiocontrolled Hydroarylation of (Trifluoromethyl)acetylenes in Superacids: Synthesis of CF3‐Substituted 1,1‐Diarylethenes
Authors: Alkhafaji Haider M. H. , Ryabukhin Dmitry S. , Muzalevskiy Vasiliy M. , Vasilyev Aleksander V. , Fukin Georgy K. , Shastin Alexey V. , Nenajdenko Valentine G. 
Published: January 2013

AbstractThe reactions between aryl(trifluoromethyl)‐substituted alkynes and arenes in triflic and fluorosulfonic acids were investigated. These reactions proceeded 100 % regioselectively to give 1,1‐diaryl‐2‐trifluoromethylethenes in high yields. Depending on the workup conditions, 3,3,3‐trifluoro‐1,1‐diarylpropan‐1‐ol was also detected in the product mixture. The reaction mechanism was studied by both spectroscopic and theoretical methods. The highly reactive nature of the trifluoromethylated vinyl cations was confirmed by DFT calculations. The stable 2,2,2‐trifluoroethylated carbocation reaction intermediates were observed by 1H, 13C, and 19F NMR spectroscopy. Under treatment with aluminium bromide, the reaction of 3,3,3‐trifluoro‐1‐phenylpropyne with benzene formed 1,3,3‐triphenylindene. The hydration of aryl(trifluoromethyl) alkynes in sulfuric or trifluoroacetic acids smoothly produced 2,2,2‐trifluoroethyl ketones in high yields.
Total Synthesis of the Spirocyclic Oxindole Alkaloids Corynoxine, Corynoxine B, Corynoxeine, and Rhynchophylline
Authors: Wanner Martin J. , Ingemann Steen , van Maarseveen Jan H. , Hiemstra Henk 
Published: January 2013

AbstractRacemic total syntheses of four spirocyclic oxindole alkaloids are reported. The general starting material was an N‐2‐butenylated 2‐hydroxytryptamine, which underwent a base‐mediated Mannich spirocyclisation with a functionalised aldehyde to generate the C‐ring. The second key step was a Pd‐catalysed cyclisation of an α‐keto ester enolate (in the original aldehyde) onto an allylic carbonate (in the N‐substituent) to form the D‐ring. The stereoselectivities of the key steps were moderate, but the isomers were readily purified, so that the natural products could be conveniently prepared, three of them for the first time.
Noni juice reduces lipid peroxidation–derived DNA adducts in heavy smokers
Authors: Wang Mian‐Ying , Peng Lin , Jensen Claude J. , Deng Shixin , West Brett J. 
Published: January 2013

AbstractFood plants provide important phytochemicals which help improve or maintain health through various biological activities, including antioxidant effects. Cigarette smoke–induced oxidative stress leads to the formation of lipid hydroperoxides (LOOHs) and their decomposition product malondialdehyde (MDA), both of which cause oxidative damage to DNA. Two hundred forty‐five heavy cigarette smokers completed a randomized, double‐blind, placebo‐controlled clinical trial designed to investigate the effect of noni juice on LOOH‐ and MDA‐DNA adducts in peripheral blood lymphocytes (PBLs). Volunteers drank noni juice or a fruit juice placebo every day for 1 month. DNA adducts were measured by 32P postlabeling analysis. Drinking 29.5–118 mL of noni juice significantly reduced adducts by 44.6–57.4%. The placebo, which was devoid of iridoid glycosides, did not significantly influence LOOH‐ and MDA‐DNA adduct levels in current smokers. Noni juice was able to mitigate oxidative damage of DNA in current heavy smokers, an activity associated with the presence of iridoids.
Estimating bulk density of compacted grains in storage bins and modifications of Janssen's load equations as affected by bulk density
Authors: Haque Ekramul 
Published: January 2013

AbstractJanssen created a classical theory based on calculus to estimate static vertical and horizontal pressures within beds of bulk corn. Even today, his equations are widely used to calculate static loadings imposed by granular materials stored in bins. Many standards such as American Concrete Institute (ACI) 313, American Society of Agricultural and Biological Engineers EP 433, German DIN 1055, Canadian Farm Building Code (CFBC), European Code (ENV 1991‐4), and Australian Code AS 3774 incorporated Janssen's equations as the standards for static load calculations on bins. One of the main drawbacks of Janssen's equations is the assumption that the bulk density of the stored product remains constant throughout the entire bin. While for all practical purposes, this is true for small bins; in modern commercial‐size bins, bulk density of grains substantially increases due to compressive and hoop stresses. Over pressure factors are applied to Janssen loadings to satisfy practical situations such as dynamic loads due to bin filling and emptying, but there are limited theoretical methods available that include the effects of increased bulk density on the loadings of grain transmitted to the storage structures. This article develops a mathematical equation relating the specific weight as a function of location and other variables of materials and storage. It was found that the bulk density of stored granular materials increased with the depth according to a mathematical equation relating the two variables, and applying this bulk‐density function, Janssen's equations for vertical and horizontal pressures were modified as presented in this article. The validity of this specific weight function was tested by using the principles of mathematics. As expected, calculations of loads based on the modified equations were consistently higher than the Janssen loadings based on noncompacted bulk densities for all grain depths and types accounting for the effects of increased bulk densities with the bed heights.
Rationing of nursing care and nurse–patient outcomes: a systematic review of quantitative studies
Authors: Papastavrou Evridiki , Andreou Panayiota , Efstathiou Georgios 
Published: January 2013

SUMMARYBedside rationing in nursing care refers to withholding or failure to carry out certain aspects of care because of limited resources such as time, staffing or skill mix. The absence of previous systematic reviews on nursing care rationing leads to a gap of synthesized knowledge on the factors and processes related to rationing and the potential negative consequences on both patients and nurses. The aim of this study was to gain an in‐depth understanding of the factors and processes related to nursing care rationing. Selected papers were methodologically assessed based on their design, sampling, measurement and statistical analysis. Seventeen quantitative studies were reviewed, and findings were categorized into four themes: elements of nursing care being rationed, causes of rationing, nurse outcomes and patient outcomes. Results revealed that communication with patients and families, patient ambulation, and mouth care were common elements of rationed care. Nurse–patient workload and communication barriers were reported as potential causes of rationing. Patient‐related outcomes included patient falls, nosocomial infections and low patient satisfaction levels. Nurse‐related outcomes included low job and occupational satisfaction. In addition, rationing appears to be an important organizational variable linked with patient safety and quality of care. This review increases understanding of what is actually occurring at the point of care delivery so that managers will be able to improve processes that lead to high quality of care and better patient and nurse outcomes. Copyright © 2013 John Wiley & Sons, Ltd.
Syndecan‐2 is a key regulator of transforming growth factor beta 2/smad2‐mediated adhesion in fibrosarcoma cells
Authors: Mytilinaiou Maria , Bano Artan , Nikitovic Dragana , Berdiaki Aikaterini , Voudouri Kallirroi , Kalogeraki Alexandra , Karamanos Nikos K. , Tzanakakis George N. 
Published: January 2013

AbstractFibrosarcoma is a rare malignant tumor originating from fibroblasts. Transforming growth factor beta 2 (TGFβ2) has been established to regulate processes correlated to fibrosarcoma tumorigenesis. In this study, we investigated the possible participation of syndecan‐2 (SDC‐2), a cell membrane heparan sulfate (HS) proteoglycan on these TGFβ2 functions. Our results demonstrate that the inhibition of SDC‐2 expression by short interfering RNA (siSDC2) abolished TGFβ2‐dependent HT1080 cell adhesion (P≤ 0.01). In parallel, the downregulation of SDC‐2 significantly inhibited TGFβ2‐induced Smad2 phosphorylation (P≤ 0.01). The immunoflourescence signal of TGF receptor III as well as its protein expression was decreased in SDC‐2‐deficient cells. The enhancement of adhesion molecules integrin β1 (P≤ 0.01) and focal adhesion kinase expression, induced by TGFβ2 treatment (P≤ 0.001), was markedly inhibited in SDC‐2‐defficient cells (P≤ 0.01). Conclusively, the obtained data suggest that SDC‐2 modulates TGFβ2 transcriptional regulation via Smad signaling to facilitate fibrosarcoma cell adhesion. © 2013 IUBMB Life, 65(2)134–143, 2013
Proteoglycans in the central nervous system: Role in development, neural repair, and Alzheimer's disease
Authors: Cui Hao , Freeman Craig , Jacobson Glenn A. , Small David H. 
Published: January 2013

AbstractProteoglycans (PGs) are major components of the cell surface and extracellular matrix and play critical roles in development and maintenance of the central nervous system (CNS). PGs are a family of proteins, all of which contain a core protein to which glycosaminoglycan side chains are covalently attached. PGs possess diverse physiological roles, particularly in neural development, and are also implicated in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease (AD). The main functions of PGs in the CNS are reviewed as are the roles of PGs in brain injury and in the development or treatment of AD. © 2013 IUBMB Life, 65(2)108–120, 2013.
ERα regulates lipid metabolism in bone through ATGL and perilipin
Authors: Wend Korinna , Wend Peter , Drew Brian G. , Hevener Andrea L. , Miranda‐Carboni Gustavo A. , Krum Susan A. 
Published: January 2013

AbstractA decrease in bone mineral density during menopause is accompanied by an increase in adipocytes in the bone marrow space. Ovariectomy also leads to accumulation of fat in the bone marrow. Herein we show increased lipid accumulation in bone marrow from estrogen receptor alpha (ERα) knockout (ERαKO) mice compared to wild‐type (WT) mice or estrogen receptor beta (ERβ) knockout (ERβKO) mice. Similarly, bone marrow cells from ERαKO mice differentiated to adipocytes in culture also have increased lipid accumulation compared to cells from WT mice or ERβKO mice. Analysis of individual adipocytes shows that WT mice have fewer, but larger, lipid droplets per cell than adipocytes from ERαKO or ERβKO animals. Furthermore, higher levels of adipose triglyceride lipase (ATGL) protein in WT adipocytes correlate with increased lipolysis and fewer lipid droplets per cell and treatment with 17β‐estradiol (E2) potentiates this response. In contrast, cells from ERαKO mice display higher perilipin protein levels, promoting lipogenesis. Together these results demonstrate that E2 signals via ERα to regulate lipid droplet size and total lipid accumulation in the bone marrow space in vivo. J. Cell. Biochem. 114: 1306–1314, 2013. © 2012 Wiley Periodicals, Inc.
MiR‐199b‐5p targets HER2 in breast cancer cells
Authors: Fang Chen , Zhao Yu , Guo Baoyu 
Published: January 2013

AbstractHER2 (ErbB2) has been reported to be overexpressed in 20–30% of breast cancer and confers poor survival because of high proliferation and metastasis rates. MicroRNAs are small noncoding RNAs that are responsible for the post‐transcriptional regulation of target genes. We found miR‐199b‐5p inhibited HER2 expression by direct targeting its 3′‐untranslated region (3′UTR) in breast cancer cells. In addition, miR‐199b‐5p inhibited HER2 downstream signaling by ERK1/2 and AKT pathways in breast cancer cells. Besides, transwell migration, wound healing, and clonogenicity were obviously inhibited by overexpression of miR‐199b‐5p in HER2‐positive breast cancer cells. We also found that miR‐199b‐5p could enhance the suppression of trastuzumab on cell migration and clonogenicity. These results suggest that miR‐199b‐5p may have the potential to be a novel important alternative therapeutic target for HER2‐positive breast cancer. J. Cell. Biochem. 114: 1457–1463, 2013. © 2013 Wiley Periodicals, Inc.
MicroRNA‐182 promotes cell growth, invasion, and chemoresistance by targeting programmed cell death 4 (PDCD4) in human ovarian carcinomas
Authors: Wang Yu‐Quan , Guo Ren‐De , Guo Rui‐Meng , Sheng Wei , Yin Li‐Rong 
Published: January 2013

AbstractAs an important tumor suppressor, programmed cell death 4 (PDCD4) influences transcription and translation of multiple genes, and modulates different signal transduction pathways. However, the upstream regulation of this gene is largely unknown. In this study, we found that microRNA‐182 (miRNA‐182, miR‐182) was upregulated, whereas PDCD4 was downregulated in ovarian cancer tissues and cell lines. Blocking or increase of miR‐182 in ovarian cancer cell lines led to an opposite alteration of endogenous PDCD4 protein level. Using fluorescent reporter assay, we confirmed the direct and negative regulation of PDCD4 by miR‐182, which was dependent on the predicted miR‐182 binding site within PDCD4 3′ untranslated region (3′ UTR). MTT and colony formation assays suggested that miR‐182 blockage suppressed, whereas miR‐182 mimics enhanced viability and colony formation of ovarian cancer cells. These effects may partly be attributed to the cell cycle promotion activity of miR‐182. miR‐182 also contributed to migration and invasion activities of ovarian cancer cells. Furthermore, miR‐182 reduced the chemosensitivity of ovarian cancer cells to CDDP and Taxol, possibly by its anti‐apoptosis activity. Importantly, all the alterations of the above cellular phenotypes by blocking or enhancing of miR‐182 could be alleviated by subsequent suppression or ectopic expression of its target PDCD4, respectively. We conclude that in ovarian cancer cells, miR‐182 acts as an oncogenic miRNA by directly and negatively regulating PDCD4. J. Cell. Biochem. 114: 1464–1473, 2013. © 2013 Wiley Periodicals, Inc.
Topology, glycosylation and conformational changes in the membrane domain of the vacuolar H+‐ATPase a subunit
Authors: Kartner Norbert , Yao Yeqi , Bhargava Ajay , Manolson Morris F. 
Published: January 2013

AbstractPublished topological models of the integral membrane a subunit of the vacuolar proton‐translocating ATPase complex have not been in agreement with respect to either the number of transmembrane helices within the integral membrane domain, or their limits and orientations within the lipid bilayer. In the present work we have constructed a predictive model of the membrane insertion of the yeast a subunit, Vph1p, from a consensus of seven topology prediction algorithms. The model was tested experimentally using epitope tagging, green fluorescent protein fusion, and protease accessibility analysis in purified yeast vacuoles. Results suggest that a consensus prediction of eight transmembrane helices with both the amino‐terminus and carboxyl‐terminus in the cytoplasm is correct. Characterization of two glycosylation sites within the homologous mouse a subunit membrane domain further corroborates this topology. Moreover, the model takes into account published data on cytoplasmic and luminal accessibility of specific amino acids. Changes in the degree of protease accessibility in response to the V‐ATPase substrate, MgATP, and the V‐ATPase‐specific inhibitor, concanamycin A, suggest that functional conformational changes occur in the large cytoplasmic loop between TM6 and TM7 of Vph1p. These data substantially confirm one topological model of the V‐ATPase a subunit and support the notion that conformational changes occur within the membrane domain, possibly involving previously proposed axial rotation and/or linear displacement of TM7 in the proton transport cycle. J. Cell. Biochem. 114: 1474–1487, 2013. © 2013 Wiley Periodicals, Inc.
HDAC inhibitor DWP0016 activates p53 transcription and acetylation to inhibit cell growth in U251 glioblastoma cells
Authors: Jin Hui , Liang Lei , Liu Lifeng , Deng Weiping , Liu Jianwen 
Published: January 2013

AbstractHere we report a hydroacid named DWP0016, which exhibited HDAC inhibition and induced p53 acetylation in U251 glioblastoma cells. DWP0016 effectively inhibited the cell growth of U251 cells and other four carcinoma cell lines but did not affect the normal cells. Cell cycle distribution analysis showed DWP0016 arrested at G1 phase cell cycle dose‐dependently in U251 cells. DWP0016 induced caspase‐dependent and independent apoptosis in U251 cells, which was identified by flow cytometry analysis, caspases activity analysis, Western blotting assay, and caspases inhibition. Mechanisms research suggested that DWP0016 activated transcription and acetylation of tumor suppressor p53. DWP0016 regulated p300, CBP, and PCAF to facilitate p53 acetylation at lys382 in U251 cells. In addition, activation of p53 by DWP0016 promoted PUMA to catalyze mitochondrial pathway. Besides, siRNA assay indicated p53 was the key gene to induce growth inhibition, cell cycle arrest, and apoptosis in DWP0016 treated U251 cells. Conclusively, our results show DWP0016 is a potent HDAC inhibitor and the anti‐tumor activity is consistent with its intended p53 activation mechanisms. These findings indicate the promising antitumor potential of DWP0016 for further glioblastoma treatment applications. J. Cell. Biochem. 114: 1498–1509, 2013. © 2013 Wiley Periodicals, Inc.
Platelet‐derived growth factor‐BB accelerates prostate cancer growth by promoting the proliferation of mesenchymal stem cells
Authors: Cheng Jiwen , Ye Huama , Liu Zhiyong , Xu Chuanliang , Zhang Zhensheng , Liu Yan , Sun Yinghao 
Published: January 2013

AbstractMesenchymal stem cells (MSCs) favor cancer growth by facilitating immunosuppression status in tumor microenvironment. However, the function and mechanism of MSCs in initiating and developing prostate cancer remains to be fully understood. In this study, we first found that MSCs promoted prostate cancer (PCa) tumor growth in vivo and cell proliferation in vitro by using PCs cell strain RM‐1. Both exogenous and endogenous MSCs could be recruited into the tumor microenvironment by using bone‐marrow transplantation model. We further demonstrated that PDGF‐BB produced by RM‐1 cell promoted MSCs proliferation in vivo and in vitro, which was abrogated by Si‐RNA specific to PDGF‐BB. And inflammatory cytokines, such as interferon gamma, tumor necrosis factor alpha, and anti‐inflammatory cytokine transformation growth factor alpha, further increased the ability of RM‐1 to produce PDGF‐BB. Overall, PCa cells produced PDGF‐BB favors the proliferation of MSCs, which may elicit immunosuppressive function and enable PCa cells to escape from the immunity surveillance in tumor inflammatory microenvironment. J. Cell. Biochem. 114: 1510–1518, 2013. © 2013 Wiley Periodicals, Inc.
Translational control of JunB, an AP‐1 transcription factor, in activated human endothelial cells
Authors: Schmid Douglas I. , Schwertz Hansjörg , Jiang Huimiao , Campbell Robert A. , Weyrich Andrew S. , McIntyre Thomas M. , Zimmerman Guy A. , Kraiss Larry W. 
Published: January 2013

AbstractStimulated endothelial cells (EC) assume an activated phenotype with pro‐inflammatory and prothrombotic features, requiring new gene and protein expression. New protein synthesis in activated EC is largely regulated by transcriptional events controlled by a variety of transcription factors. However, post‐transcriptional control of gene expression also influences phenotype and allows the cell to alter protein expression in a faster and more direct way than is typically possible with transcriptional mechanisms. We sought to demonstrate that post‐transcriptional control of gene expression occurs during EC activation. Using thrombin‐activated EC and a high‐throughput, microarray‐based approach, we identified a number of gene products that may be regulated through post‐transcriptional mechanisms, including the AP‐1 transcription factor JunB. Using polysome profiling, cytoplasts and other standard cell biologic techniques, JunB is shown to be regulated at a post‐transcriptional level during EC activation. In activated EC, the AP‐1 transcription factor JunB, is regulated on a post‐transcriptional level. Signal‐dependent control of translation may regulate transcription factor expression and therefore, subsequent transcriptional events in stimulated EC. J. Cell. Biochem. 114: 1519–1528, 2013. © 2013 Wiley Periodicals, Inc.
Hydrogen sulfide reduces cell adhesion and relevant inflammatory triggering by preventing ADAM17‐dependent TNF‐α activation
Authors: Perna Alessandra F. , Sepe Immacolata , Lanza Diana , Capasso Rosanna , Zappavigna Silvia , Capasso Giovambattista , Caraglia Michele , Ingrosso Diego 
Published: January 2013

AbstractH2S is the third endogenous gaseous mediator, after nitric oxide and carbon monoxide, possessing pleiotropic effects, including cytoprotection and anti‐inflammatory action. We analyzed, in an in vitro model entailing monocyte adhesion to an endothelial monolayer, the changes induced by H2S on various potential targets, including cytokines, chemokines, and proteases, playing a crucial role in inflammation and cell adhesion. Results show that H2S prevents the increase in monocyte adhesion induced by tumor necrosis factor‐α (TNF‐α). Under these conditions, downregulation of monocyte chemoattractant protein‐1 (MCP‐1), chemokine C‐C motif receptor 2, and increase of cluster of differentiation 36 could be detected in monocytes. In endothelial cells, H2S treatment reduces the increase in MCP‐1, inter‐cellular adhesion molecule‐1, vascular cell adhesion molecule‐1, and of a disintegrin and metalloproteinase metallopeptidase domain 17 (ADAM17), both at the gene expression and protein levels. Cystathionine γ‐lyase and 3‐mercaptopyruvate sulfurtransferase, the major H2S forming enzymes, are downregulated in endothelial cells. In addition, H2S significantly reduces activation of ADAM17 by PMA in endothelial cells, with consequent reduction of both ADAM17‐dependent TNF‐α ectodomain shedding and MCP‐1 release. In conclusion, H2S is able to prevent endothelial activation by hampering endothelial activation, triggered by TNF‐α. The mechanism of this protective effect is mainly mediated by down‐modulation of ADAM17‐dependent TNF‐converting enzyme (TACE) activity with consequent inhibition of soluble TNF‐α shedding and its relevant MCP‐1 release in the medium. These results are discussed in the light of the potential protective role of H2S in pro‐inflammatory and pro‐atherogenic processes, such as chronic renal failure. J. Cell. Biochem. 114: 1536–1548, 2013. © 2013 Wiley Periodicals, Inc.