Relatos sublimes a través de objetos cotidianos : identidad, poder y cotidianidad en la obra de Eulália Valldosera

This work reflects on the work of Eulália Valldosera, (1963), through a conceptual and formal analysis. This multidisciplinary artist builds sublime stories through everyday objects. Her work explores the notions of sexual identity, love, illness and death as well as issues related to memory and the ways in which we reconstruct our own past. Valldosera forms a dialogue between lights and shadows loaded with psychoanalytic elements that immerse the viewer into an experiential process of reflection and self-knowledge all through photography, installation, performance and everyday objectsinfo:eu-repo/semantics/publishedVersio

From 'River Cottage' to 'Chicken Run': Hugh Fearnley-Whttingstall and the class politics of ethical consumption

Lifestyle television provides a key site through which to explore the dilemmas of ethical consumption, as the genre shifts to consider the ethics of different consumption practices and taste cultures. UK television cook Hugh Fearnley-Whittingstall's TV programmes offer fertile ground not only for thinking about television personalities as lifestyle experts and moral entrepreneurs, but also for thinking about how the meanings and uses of their television image are inflected by genre. In this article we explore how the shift from the lifestyled downshifting narrative of the River Cottage series to the 'campaigning culinary documentary' Hugh's Chicken Run exposes issues of celebrity, class and ethics. While both series are concerned with ethical consumption, they work in different ways to reveal a distinction between 'ethical' and 'unethical' consumption practices and positions - positions that are inevitably classed

Transient supraselective hepatic intra-arterial chemoembolization in patients with hepatocellular carcinoma or liver metastasis with controlled primary

Antecedentes: No existe tratamiento estándar para pacientes con carcinoma hepatocelular o metástasis hepática no erradicarle con primario controlado pero que han fallado al tratamiento sistémico. Se presenta la experiencia del tratamiento con quimio embolización intraarterial hepática supra selectiva (QEIAHS) realizado en la Unidad de Oncología del Hospital Universitario de Santander, Bucaramanga, Colombia. Metodología: Se revisaron las historias clínicas de los pacientes atendidos entre marzo de 2000 a marzo de 2007. Resultados: Se realizaron doce procedimientos de QEIAHS en seis pacientes (entre uno y cuatro ciclos por paciente). Cuatro tenían patología maligna propia del tejido hepático (hepatocarcinoma o colangiocarcinoma) y dos a metástasis (tumor carcinoide y adenocarcinoma de sigmoides) confinadas al hígado. El tamaño basal de las masas tumorales dominantes estaban entre 5 y 12 cm; el síntoma predominante en todos los casos fue dolor abdominal grado 2. El estado funcional al inicio era igual o mejor a 1. La respuesta se evaluó cuatro semanas después de la aplicación de cada ciclo de QEIAHS. En una paciente el procedimiento fue fallido por aterosclerosis. Las mejores respuestas paliativas alcanzadas estuvieron entre 50 y 93%, aunque en un paciente se dio progresión. Los eventos adversos fueron mínimos, transitorios y de fácil manejo médico, sin presencia de efectos hematológicos. Solo un paciente presentó síndrome postquimio embolización. El tiempo medio de de seguimiento fue de 11.2 meses, con mediana de sobrevida de 16 meses y sobrevida a 2 años de 27%. En todos los pacientes desapareció el dolor, mantuvieron estado funcional grado 0 y 1, permaneciendo activos y con buenos niveles de autocuidado durante el periodo de sobrevida, estando generalmente asintomáticos. Conclusiones: La QEIAHS de la(s) arteria(s) nutricia(s) por angiografía del tronco celiaco es una alternativa paliativa para el tratamiento de pacientes con tumores primarios hepáticos o metastásicos confinados al hígado, con efectos colaterales mínimos y buena respuesta de paliación, manteniendo un excelente estado funcional y sin dolor.[Bracho ML, Insuasty JS, Saaibi JF, Gamarra G, M`comick A. Quimioembolización intraarterial hepática supraselectiva transitoria en pacientes con hepatocarcinoma o metástasis a hígado con primario controlado. MedUNAB 2008; 11:95-102].Background: There is no standard treatment for patients with hepatocellular carcinoma or liver metastasis that cannot be eradicated with controlled primary treatment but who have failed systemic treatment. The experience of treatment with supra-selective hepatic intra-arterial chemoembolization (QEIAHS) performed in the Oncology Unit of the University Hospital of Santander, Bucaramanga, Colombia is presented. Methodology: The medical records of patients seen between March 2000 and March 2007 were reviewed. Results: Twelve QEIAHS procedures were performed in six patients (between one and four cycles per patient). Four had malignant pathology specific to the liver tissue (hepatocarcinoma or cholangiocarcinoma) and two had metastases (carcinoid tumor and sigmoid adenocarcinoma) confined to the liver. The baseline size of the dominant tumor masses was between 5 and 12 cm; the predominant symptom in all cases was grade 2 abdominal pain. The functional status at baseline was equal to or better than 1. The response was evaluated four weeks after the application of each cycle of QEIAHS. In one patient the procedure was failed due to atherosclerosis. The best palliative responses achieved were between 50 and 93%, although progression occurred in one patient. Adverse events were minimal, transient and easy to manage medically, with no hematological effects present. Only one patient presented postchemoembolization syndrome. The mean follow-up time was 11.2 months, with median survival of 16 months and 2-year survival of 27%. In all patients, the pain disappeared, they maintained functional status grade 0 and 1, remaining active and with good levels of self-care during the survival period, being generally asymptomatic. Conclusions: QEIAHS of the nutrient artery(s) by angiography of the celiac trunk is a palliative alternative for the treatment of patients with primary hepatic or metastatic tumors confined to the liver, with minimal side effects and a good palliation response. , maintaining an excellent functional status and without pain.[Bracho ML, Insuasty JS, Saaibi JF, Gamarra G, M`comick A. Transient supraselective hepatic intraarterial chemoembolization in patients with hepatocellular carcinoma or liver metastasis with a controlled primary. MedUNAB 2008; 11:95-102]

Polyphenols act synergistically with doxorubicin and etoposide in leukaemia cell lines

The study aimed to assess the effects of polyphenols when used in combination with doxorubicin and etoposide, and to determine whether polyphenols sensitised leukaemia cells, causing inhibition of cell proliferation, cell cycle arrest and induction of apoptosis. This study is based on findings in solid cancer tumours, which have shown that polyphenols can sensitize cells to chemotherapy, and induce apoptosis and/or cell-cycle arrest. This could enable a reduction of chemotherapy dose and off-target effects, whilst maintaining treatment efficacy. Quercetin, apigenin, emodin, rhein and cis-stilbene were investigated alone and in combination with etoposide and doxorubicin in two lymphoid and two myeloid leukaemia cells lines. Measurements were made of ATP levels (using CellTiter-Glo assay) as an indication of total cell number, cell cycle progression (using propidium iodide staining and flow cytometry) and apoptosis (NucView caspase 3 assay and Hoechst 33342/propidium iodide staining). Effects of combination treatments on caspases 3, 8 and 9 activity were determined using Glo luminescent assays, glutathione levels were measured using the GSH-Glo Glutathione Assay and DNA damage determined by anti-γH2AX staining. Doxorubicin and etoposide in combination with polyphenols synergistically reduced ATP levels, induced apoptosis and increased S and/or G2/M phase cell cycle arrest in lymphoid leukaemia cell lines. However, in the myeloid cell lines the effects of the combination treatments varied; doxorubicin had a synergistic or additive effect when combined with quercetin, apigenin, emodin, and cis-stilbene, but had an antagonistic effect when combined with rhein. Combination treatment caused a synergistic downregulation of glutathione levels and increased DNA damage, driving apoptosis via caspase 8 and 9 activation. However, in myeloid cells where antagonistic effects were observed, this was associated with increased glutathione levels and a reduction in DNA damage and apoptosis. This study has demonstrated that doxorubicin and etoposide activity were enhanced by polyphenols in lymphoid leukaemia cells, however, differential responses were seen in myeloid cells with antagonistic responses seen in some combination therapies

Insight into glucocorticoid receptor signalling through interactome model analysis

Glucocorticoid hormones (GCs) are used to treat a variety of diseases because of their potent anti-inflammatory effect and their ability to induce apoptosis in lymphoid malignancies through the glucocorticoid receptor (GR). Despite ongoing research, high glucocorticoid efficacy and widespread usage in medicine, resistance, disease relapse and toxicity remain factors that need addressing. Understanding the mechanisms of glucocorticoid signalling and how resistance may arise is highly important towards improving therapy. To gain insight into this we undertook a systems biology approach, aiming to generate a Boolean model of the glucocorticoid receptor protein interaction network that encapsulates functional relationships between the GR, its target genes or genes that target GR, and the interactions between the genes that interact with the GR. This model named GEB052 consists of 52 nodes representing genes or proteins, the model input (GC) and model outputs (cell death and inflammation), connected by 241 logical interactions of activation or inhibition. 323 changes in the relationships between model constituents following in silico knockouts were uncovered, and steady-state analysis followed by cell-based microarray genome-wide model validation led to an average of 57% correct predictions, which was taken further by assessment of model predictions against patient microarray data. Lastly, semi-quantitative model analysis via microarray data superimposed onto the model with a score flow algorithm has also been performed, which demonstrated significantly higher correct prediction ratios (average of 80%), and the model has been assessed as a predictive clinical tool using published patient microarray data. In summary we present an in silico simulation of the glucocorticoid receptor interaction network, linked to downstream biological processes that can be analysed to uncover relationships between GR and its interactants. Ultimately the model provides a platform for future development both by directing laboratory research and allowing for incorporation of further components, encapsulating more interactions/genes involved in glucocorticoid receptor signalling

DNA damage precedes apoptosis during the regression of the interdigital tissue in vertebrate embryos

DNA damage independent of caspase activation accompanies programmed cell death in different vertebrate embryonic organs. We analyzed the significance of DNA damage during the regression of the interdigital tissue, which sculpts the digits in the embryonic limb. Interdigit remodeling involves oxidative stress, massive apoptosis and cell senescence. Phosphorylation of H2AX mediated by ATM precedes caspase dependent apoptosis and cell senescence during interdigit regression. The association of ?H2AX with other downstream DNA repair factors, including MDC1, Rad50 and 53BP1 suggests a defensive response of cells against DNA damage. The relative distribution of cells ?H2AX-only positive, TUNEL-only positive, and cells double positive for both markers is consistent with a sequence of degenerative events starting by damage of the DNA. In support of this interpretation, the relative number of ?H2AX-only cells increases after caspase inhibition while the relative number of TUNELonly cells increases after inhibition of ATM. Furthermore, cultured interdigits survived and maintained intense chondrogenic potential, even at advanced stages of degeneration, discarding a previous commitment to die. Our findings support a new biological paradigm considering embryonic cell death secondary to genotoxic stimuli, challenging the idea that considers physiological cell death a cell suicide regulated by an internal death clock that pre-programmes degeneration

Chromatin Structure Following UV-Induced DNA Damage—Repair or Death?

In eukaryotes, DNA is compacted into a complex structure known as chromatin. The unravelling of DNA is a crucial step in DNA repair, replication, transcription and recombination as this allows access to DNA for these processes. Failure to package DNA into the nucleosome, the individual unit of chromatin, can lead to genomic instability, driving a cell into apoptosis, senescence, or cellular proliferation. Ultraviolet (UV) radiation damage causes destabilisation of chromatin integrity. UV irradiation induces DNA damage such as photolesions and subjects the chromatin to substantial rearrangements, causing the arrest of transcription forks and cell cycle arrest. Highly conserved processes known as nucleotide and base excision repair (NER and BER) then begin to repair these lesions. However, if DNA repair fails, the cell may be forced into apoptosis. The modification of various histones as well as nucleosome remodelling via ATP-dependent chromatin remodelling complexes are required not only to repair these UV-induced DNA lesions, but also for apoptosis signalling. Histone modifications and nucleosome remodelling in response to UV also lead to the recruitment of various repair and pro-apoptotic proteins. Thus, the way in which a cell responds to UV irradiation via these modifications is important in determining its fate. Failure of these DNA damage response steps can lead to cellular proliferation and oncogenic development, causing skin cancer, hence these chromatin changes are critical for a proper response to UV-induced injury

Saturation Diving Alters Folate Status and Biomarkers of DNA Damage and Repair

Exposure to oxygen-rich environments can lead to oxidative damage, increased body iron stores, and changes in status of some vitamins, including folate. Assessing the type of oxidative damage in these environments and determining its relationships with changes in folate status are important for defining nutrient requirements and designing countermeasures to mitigate these effects. Responses of humans to oxidative stressors were examined in participants undergoing a saturation dive in an environment with increased partial pressure of oxygen, a NASA Extreme Environment Mission Operations mission. Six participants completed a 13-d saturation dive in a habitat 19 m below the ocean surface near Key Largo, FL. Fasting blood samples were collected before, twice during, and twice after the dive and analyzed for biochemical markers of iron status, oxidative damage, and vitamin status. Body iron stores and ferritin increased during the dive (P<0.001), with a concomitant decrease in RBC folate (P<0.001) and superoxide dismutase activity (P<0.001). Folate status was correlated with serum ferritin (Pearson r = −0.34, P<0.05). Peripheral blood mononuclear cell poly(ADP-ribose) increased during the dive and the increase was significant by the end of the dive (P<0.001); γ-H2AX did not change during the mission. Together, the data provide evidence that when body iron stores were elevated in a hyperoxic environment, a DNA damage repair response occurred in peripheral blood mononuclear cells, but double-stranded DNA damage did not. In addition, folate status decreases quickly in this environment, and this study provides evidence that folate requirements may be greater when body iron stores and DNA damage repair responses are elevated