Privatising culture: aspects of corporate intervention in contemporary art and art institutions during the Reagan and Thatcher decade

This study provides an analysis of the growth of corporate art intervention in America and Britain during the Reagan-Thatcher era of the 1980s. The premise is that the factors governing business intervention into the art world are inseparable from the free-market enterprise culture and the government-specific policies deployed to promote it. After a general introduction, Chapter 2 investigates the concept of the state and its role in relation to the arts. The public perception of differences between the American and British arts funding systems is further explored in terms of the financing of American art museums, and the arts provision provided by the state before the 1980s is examined in the practices of the Arts Council of Great Britain and the National Endowment for the Arts. The public arts policies of the New Right, and in particular the use of tax deduction incentives, are analysed in Chapter 3. It also examine the host of measures implemented by the two governments to inject the principles and ethos of the free market into these public arts agencies, and to transform them into paragons of arts privatisation. The corporate takeover of art museums is the subject of Chapter 4. The crucial role played by the corporate elites who served on the boards of trustees of these institutions is investigated, together with the great influx of corporate capital into them. Chapter 5 gives an account of how corporations integrated themselves into the arts support system, by holding art exhibitions themselves, and by establishing branches of public art museums within corporate premises. Chapter 6, which concentrates on corporate art collections themselves, shows how these came to fulfil the dual function of private investment and public image-enhancing, how they sought and achieved validation and legitimation, how artists reacted to them, and how they succeeded in re-defining the meaning of cultural production. A conclusion summarises the various developments of corporate art intervention under the "casino economy" of the Reagan-Thatcher decade, and looks forward to possible directions for the future

Interactions Between Reinforcement Corrosion and Chloride Ion Diffusion in Mortar

This study explored the diffusion of the chloride ions influenced by the reinforcement corrosion in the mortar. It is believed that, during the corroding process, a small current is generated at the surface of the reinforcement. Such current is supposed to influence the diffusion of the chloride ions, but the relationship between both was not well studied in the literature. In this study, the corroded reinforcements were prepared by applied currents. Reinforced mortar specimens with w/c of 0.6 were then prepared and cured by either salt or fresh water. Results showed that the chloride ion distribution was likely associated with the reinforcement corrosion. During the early hydration, the chloride ions were attracted by the reinforcement corrosion in the specimens prepared with fresh water and cured in salt water. The concentration of the chloride ions near the surface of the reinforcement was increased with the increases of the charging time during the preparation for the corroded reinforcement. On the contrary, the chloride ions were likely bound in those specimens prepared with salt water and cured by saturated lime water. The concentration of the chloride ions near the surface of the reinforcement was higher than those near the outer surface. However, such influencing effects were not clear in the long term, possibly due to the hydration. The results of this study show that the reinforcement corrosion have influences on the diffusion of the chloride ions and such effect should be considered during the refinement of the traditional chloride ion diffusion models

Nucleostemin and GNL3L exercise distinct functions in genome protection and ribosome synthesis, respectively

The mammalian nucleolar proteins nucleostemin (NS) and GNL3L (for GNL3-like) are encoded by paralogous genes that arose from an invertebrate ancestral gene, GNL3. Invertebrate GNL3 has been implicated in ribosome biosynthesis as has its mammalian descendent GNL3L, whereas the paralogous mammalian NS gene has instead been implicated in cell renewal. Here we found that NS depletion in a human breast carcinoma cell line triggered a prompt and significant effect of DNA damage in S-phase cells without perturbing the initial step of rRNA synthesis and only mildly affected the total ribosome production. In contrast, GNL3L depletion markedly impaired ribosome production without inducing appreciable DNA damage. These results indicate that during vertebrate evolution GNL3L retained the role of the ancestral gene in ribosome biosynthesis while the paralogous NS acquired a novel genome-protective function. Our results provide a coherent explanation for what had seemed to be contradictory findings about the functions of the invertebrate vs. vertebrate genes, and also speak to how the nucleolus was fine-tuned for a role in genome protection and cell cycle control as the vertebrates evolved.</jats:p

Robust PID based indirect-type iterative learning control for batch processes with time-varying uncertainties

ased on the proportional-integral-derivative (PID) control structure widely used in engineering applications, a robust indirect-type iterative learning control (ILC) method is proposed for industrial batch processes subject to time-varying uncertainties. An important merit is that the proposed ILC design is independent of the PID tuning that aims primarily to hold robust stability of the closed-loop system, owing to the fact that the ILC updating law is implemented through adjusting the setpoint of the closed-loop PID control structure plus a feedforward control to the plant input from batch to batch. According to the robust H infinity control objective, a robust discrete-time PID tuning algorithm is given in terms of the plant state-space model description to accommodate for time-varying process uncertainties. For the batchwise direction, a robust ILC updating law is developed based on the two-dimensional (2D) control system theory. Only measured output errors of current and previous cycles are used to implement the proposed ILC scheme for the convenience of practical application. An illustrative example from the literature is adopted to demonstrate the effectiveness and merits of the proposed ILC method

Tamoxifen resistance in breast cancer is regulated by the EZH2–ERa–GREB1 transcriptional axis

Resistance to cancer treatment can be driven by epigenetic reprogramming of specific transcriptomes in favor of the refractory phenotypes. Here we discover that tamoxifen resistance in breast cancer is driven by a regulatory axis consisting of a master transcription factor, its cofactor, and an epigenetic regulator. The oncogenic histone methyltransferase EZH2 conferred tamoxifen resistance by silencing the expression of the estrogen receptor a (ERa) cofactor GREB1. In clinical specimens, induction of DNA methylation of a particular CpG-enriched region at the GREB1 promoter negatively correlated with GREB1 levels and cell sensitivity to endocrine agents. GREB1 also ensured proper cellular reactions to different ligands by recruiting distinct sets of ERa cofactors to cis-regulatory elements, which explains the contradictory biological effects of GREB1 on breast cancer cell growth in response to estrogen or antiestrogen. In refractory cells, EZH2-dependent repression of GREB1 triggered chromatin reallocation of ERa coregulators, converting the antiestrogen into an agonist. In clinical specimens from patients receiving adjuvant tamoxifen treatment, expression levels of EZH2 and GREB1 were correlated negatively, and taken together better predicted patient responses to endocrine therapy. Overall, our work suggests a new strategy to overcome endocrine resistance in metastatic breast cancer by targeting a particular epigenetic program. Significance: This study suggests a new strategy to overcome endocrine resistance in metastatic breast cancer by targeting a particular epigenetic program defined within.Fil: Wu, Yanming. University of Texas at San Antonio; Estados UnidosFil: Zhang, Zhao. University of Texas at San Antonio; Estados UnidosFil: Cenciarini, Mauro Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Proietti Anastasi, Cecilia Jazmín. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Amasino, Matías Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Hong, Tao. University of Texas at San Antonio; Estados Unidos. Central South University; ChinaFil: Yang, Mei. University of Texas at San Antonio; Estados UnidosFil: Liao, Yiji. University of Texas at San Antonio; Estados UnidosFil: Chiang, Huai-Chin. University of Texas at San Antonio; Estados Unidos. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio;Fil: Kaklamani, Virginia G.. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio;Fil: Jeselsohn, Rinath. Dana-farber Cancer Institute; Estados UnidosFil: Vadlamudi, Ratna K.. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio;Fil: Huang, Tim Hui Ming. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio;Fil: Li, Rong. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio;Fil: De Angelis, Carmine. Baylor College Of Medicine; Estados UnidosFil: Fu, Xiaoyong. Baylor College Of Medicine; Estados UnidosFil: Elizalde, Patricia Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Schiff, Rachel. Baylor College Of Medicine; Estados UnidosFil: Brown, Myles. Dana farber Cancer Institute; Estados UnidosFil: Xu, Kexin. University Of Texas Health Science Center At San Antonio (ut Health San Antonio) ; University Of Texas At San Antonio

Application of UV absorbance and fluorescence indicators to assess the formation of biodegradable dissolved organic carbon and bromate during ozonation

This study examined the significance of changes of UV absorbance and fluorescence of dissolved organic matter (DOM) as surrogate indicators for assessing the formation of bromate and biodegradable dissolved organic carbon (BDOC) during the ozonation of surface water and wastewater effluent. Spectroscopic monitoring was carried out using benchtop UV/Vis and fluorescence spectrophotometers and a newly developed miniature LED UV/fluorescence sensor capable of rapidly measuring UVA280 and protein-like and humic-like fluorescence. With the increase of O3/DOC mass ratio, the plots of BDOC formation were characterized of initial lag, transition slope and final plateau. With the decrease of UV absorbance and fluorescence, BDOC concentrations initially increased slowly and then rose more noticeably. Inflection points in plots of BDOC versus changes of spectroscopic indicators were close to 35 e45% loss of UVA254 or UVA280 and 75e85% loss of humic-like fluorescence. According to the data from size exclusion chromatography (SEC) with organic carbon detection and 2D synchronous correlation analyses, DOM fractions assigned to operationally defined large biopolymers (apparent molecular weight, AMW>20 kDa) and medium AMW humic substances (AMW 5.5e20 kDa) were transformed into medium-size building blocks (AMW 3e5.5 kDa) and other smaller AMW species (AMW<3 kDa) associated with BDOC at increasing O3/DOC ratios. Appreciable bromate formation was observed only after the values of UVA254, UVA280 and humic-like fluorescence in O3-treated samples were decreased by 45 e55%, 50e60% and 86e92% relative to their respective initial levels. No significant differences in plots of bromate concentrations versus decreases of humic-like fluorescence were observed for surface water and wastewater effluent samples. This was in contrast with the plots of bromate concentration versus UVA254 and UVA280 which exhibited sensitivity to varying initial bromide concentrations in the investigated water matrixes. These results suggest that measurements of humic-like fluorescence can provide a useful supplement to UVA indices for characterization of ozonation processes

3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

Lesions of ERBB2, PTEN, and PIK3CA activate the phosphati- dylinositol 3-kinase (PI3K) pathway during cancer development by increasing levels of phosphatidylinositol-3,4,5-triphosphate (PIP3). 3-Phosphoinositide-dependent kinase 1 (PDK1) is the first node of the PI3K signal output and is required for activation of AKT. PIP3 recruits PDK1 and AKT to the cell membrane through interactions with their pleckstrin homology domains, allowing PDK1 to activate AKT by phosphorylating it at residue threonine-308. We show that total PDK1 protein and mRNA were overexpressed in a majority of human breast cancers and that 21% of tumors had five or more copies of the gene encoding PDK1, PDPK1. We found that increased PDPK1 copy number was associated with upstream pathway lesions (ERBB2 amplification, PTEN loss, or PIK3CA mutation), as well as patient survival. Examination of an independent set of breast cancers and tumor cell lines derived from multiple forms of human cancers also found increased PDK1 protein levels associated with such upstream pathway lesions. In human mammary cells, PDK1 enhanced the ability of upstream lesions to signal to AKT, stimulate cell growth and migration, and rendered cells more resistant to PDK1 and PI3K inhibition. After orthotopic transplantation, PDK1 overexpression was not oncogenic but dramatically enhanced the ability of ERBB2 to form tumors. Our studies argue that PDK1 overexpression and increased PDPK1 copy number are common occurrences in cancer that potentiate the oncogenic effect of upstream lesions on the PI3K pathway. Therefore, we conclude that alteration of PDK1 is a critical component of oncogenic PI3K signaling in breast cancer

Tissue-specific gene expression templates for accurate molecular characterization of the normal physiological states of multiple human tissues with implication in development and cancer studies

<p>Abstract</p> <p>Background</p> <p>To elucidate the molecular complications in many complex diseases, we argue for the priority to construct a model representing the normal physiological state of a cell/tissue.</p> <p>Results</p> <p>By analyzing three independent microarray datasets on normal human tissues, we established a quantitative molecular model GET, which consists of 24 tissue-specific <it>G</it>ene <it>E</it>xpression <it>T</it>emplates constructed from a set of 56 genes, for predicting 24 distinct tissue types under disease-free condition. 99.2% correctness was reached when a large-scale validation was performed on 61 new datasets to test the tissue-prediction power of GET. Network analysis based on molecular interactions suggests a potential role of these 56 genes in tissue differentiation and carcinogenesis.</p> <p>Applying GET to transcriptomic datasets produced from tissue development studies the results correlated well with developmental stages. Cancerous tissues and cell lines yielded significantly lower correlation with GET than the normal tissues. GET distinguished melanoma from normal skin tissue or benign skin tumor with 96% sensitivity and 89% specificity.</p> <p>Conclusions</p> <p>These results strongly suggest that a normal tissue or cell may uphold its normal functioning and morphology by maintaining specific chemical stoichiometry among genes. The state of stoichiometry can be depicted by a compact set of representative genes such as the 56 genes obtained here. A significant deviation from normal stoichiometry may result in malfunction or abnormal growth of the cells.</p

A Novel Tetrameric PilZ Domain Structure from Xanthomonads

PilZ domain is one of the key receptors for the newly discovered secondary messenger molecule cyclic di-GMP (c-di-GMP). To date, several monomeric PilZ domain proteins have been identified. Some exhibit strong c-di-GMP binding activity, while others have barely detectable c-di-GMP binding activity and require an accessory protein such as FimX to indirectly respond to the c-di-GMP signal. We now report a novel tetrameric PilZ domain structure of XCC6012 from the plant pathogen Xanthomonas campestris pv. campestris (Xcc). It is one of the four PilZ domain proteins essential for Xcc pathogenicity. Although the monomer adopts a structure similar to those of the PilZ domains with very weak c-di-GMP binding activity, it is nevertheless interrupted in the middle by two extra long helices. Four XCC6012 proteins are thus self-assembled into a tetramer via the extra heptad repeat α3 helices to form a parallel four-stranded coiled-coil, which is further enclosed by two sets of inclined α2 and α4 helices. We further generated a series of XCC6012 variants and measured the unfolding temperatures and oligomeric states in order to investigate the nature of this novel tetramer. Discovery of this new PilZ domain architecture increases the complexity of c-di-GMP-mediated regulation