La fachada como lugar en la arquitectura contemporánea

La tesis se articula en tres capítulos, estructurados siguiendo un proceso de extensión espacio temporal paralelo al que incumbe al cuerpo propio, entendiendo por tanto la fachada, es decir el rostro de la arquitectura (facies), como proyección directa de nuestra exterioridad y punto de registro de las alteraciones que afectan tanto a nuestra corporeidad como al objeto arquitectónico y al paisaje natural y urbano contemporáneo. El cuerpo, su esqueleto, su piel, su rostro, y las diferentes máscaras que filtran su relación con el mundo, se convierten en la clave para una lectura interdisciplinar de las mutaciones que se registran en las fronteras arquitectónicas. La extensión espacio temporal del cuerpo es el punto de partida de la investigación y la estructura misma de la tesis que se desarrolla con el siguiente criterio: la fachada en relación con el rostro y el cuerpo propio (relación: cuerpo arquitectura, rostro- fachada); la fachada en relación con el edificio; su separación y autonomía formal, estructural y comunicativa (relación: piel esqueleto; estructura revestimiento). la fachada con respecto al nuevo paisaje natural y urbano (rostro paisaje; fachada nueva ecología, en un contexto de hibridación tecnológica y artificialización del mundo). En el primer capítulo partimos portante del cuerpo propio, entendiendo que las diferentes formas, fachadas o rostros que vestidos, cosas y casas adquieren en el tiempo, son proyecciones directas de nuestra exterioridad en un proceso de extensión espacio temporal que es también un proceso de significación. Como ya avisaba Ortega, todas las extensiones del hombre, es decir los productos de la técnica y de la industria que el hombre construye para adaptarse a diferentes condiciones de vida, se convierten en instrumentos para clasificar socialmente una persona, y son por tanto máscaras o "estilos" que revelan las épocas correspondientes. Por La máscara y sus diferentes connotaciones se convierten en medios para analizar un proceso que nos sitúa finalmente en la "máscara electrónica", es decir una piel híbrida, mejorada y extendida hasta los límites propios del mundo, que responde a los cambios impuestos por la moda y a los devenires cada vez más acelerados. En el segundo capítulo nos situamos en la piel del objeto arquitectónico y en su proceso de desvinculación formal, estructural y comunicativo de la estructura, en un debate abierto con diferentes connotaciones entre revelar y enmascarar El proceso pasa por diferentes momentos históricos, destacando: el Renacimiento, como momento en el que se forja el término fachada, como resultado de una determinada manera de entender la representación arquitectónica, social y urbana; la Revolución Industrial, por la introducción de los nuevos materiales y sistemas de producción y consumo que se materializan en las Grandes Exposiciones Universales; finalmente la Posmodernidad, como momento en el que se forjan las bases de la "superficialidad posmoderna", como Jameson la define, desde el presupuesto de una necesidad de símbolos y significados que justifica las actitudes formales propias del final del siglo XX y las alteraciones en el límite que se perfilan en el nuevo milenio. En el tercer capítulo se investigan las consecuencias de esta desvinculación a nivel del paisaje natural y urbano, en una perspectiva de hibridación planetaria que pone en cuestión las clasificaciones tradicionales. La fachada es finalmente interfaz, término de raíz informática, que indica en sí mismo las alteraciones que afectan al límite, convertido en lugar, membrana osmótica y filtro de informaciones. La interfaz es una máscara pues, como la definición indica, remite al intercambio de información pero no al proceso que dicho intercambio determina El límite es por tanto un lugar, una entidad ensanchada e indeterminada en la que ocurren intercambios e interacciones que sólo se revelan a pocos selectos y que tienen en definitiva que quedar ocultas. En este lugar nos situamos para analizar las alteraciones contemporáneas que afectan a nuestras ciudades, objeto, como la piel del cuerpo propio, de la colonización despiadada del consumo de masa y de la tecnología electrónica. Por un lado el fascinante mundo interconectado y fluido de las redes y por otro lado ciudades cada vez más fragmentadas en las que los límites se multiplican, obligando a situamos con nuevas actitudes frente a un paisaje y a una naturaleza controlados con diferentes grados de manipulación. Si la fachada en su acepción tradicional suponía una actitud de continuidad urbana y de respecto de reglas compositivas determinadas, la piel es un territorio más abierto y flexible, que puede ser camuflado, enmascarado, desmaterializado con diferentes estrategias que son en definitiva respuestas a la dilatación y proliferación de los límites y a las necesidades de una sociedad en la que predomina el control en todas sus acepciones. La fachada tradicional aislaba, protegía y filtraba prudentemente las relaciones entre la esfera pública y la privada, al tiempo que revelaba el estatus y el rol de cada edificio en su contexto. La anulación de la fachada en la modernidad, tanto a nivel del objeto arquitectónico como de la ciudad misma, supone una actitud de rechazo frente a la máscara y la contraposición edificio - paisaje como entidades autónomas. El artefacto arquitectónico se concibe como objeto aislado y la propia ciudad crece de manera exacerbada anulando el sentido de la fachada tradicional. Hoy la sustitución de la fachada por la interfaz no deriva de una actitud moralista, pues la ética ha sido anulada por una estetización que ocupa todos los niveles de la sociedad y de la vida. Asumimos que la máscara, como ya decía Semper, siempre es necesaria, pero si la fachada era máscara social, la interfaz es una máscara electrónica, piel híbrida capaz de ser infinitamente colonizada y de responder a las exigencias de cambio que impone el mundo en el que vivimos. El campo de investigación queda abierto, perfilándose la posibilidad de imaginar una arquitectura menos preocupada por efectos formales y espectaculares, y más centrada hacia las posibilidades que ofrece la electrónica en su aplicación a la arquitectura como respuesta a las exigencias del hombre contemporáneo.

O BOCA A BOCA ON-LINE: AS IMPLICAÇÕES DA VOZ DO CONSUMIDOR NA COMUNICAÇÃO DE MERCADO

O consumidor contemporâneo, inserido em um novo ambiente de comunicação, potencializa suas expressões, capaz de avaliar uma marca ou produto e transmitir sua opinião pelas redes sociais, ou seja, o consumidor expressa suas opiniões e desejos dialogando com seus pares de forma espontânea nas redes sociais on-line. É neste ambiente de participação e interação (ciberespaço) que está nosso objeto de estudo, o boca a boca on-line – a voz do consumidor contemporâneo, também conhecido como uma manifestação informativa pessoal ou uma conversa, a opinion sharing. Proporcionado pelos consumidores nas redes sociais on-line, o boca a boca se fortalece em função das possibilidades de interação, característica da sociedade em rede. Nesse cenário, oobjetivo desta pesquisa é caracterizar o boca a boca on-line como um novo fluxo comunicacional entre consumidores, hoje potencializado pelas novas tecnologias da comunicação, capazes de alterar a percepção da marca e demonstrar o uso, pelas marcas, das redes sociais on-line ainda como um ambiente de comunicação unidirecional. Mediante três casos selecionados por conveniência (dois casos nacionais e um internacional), o corpus de análise de nossa pesquisa se limitou aos 5.084 comentários disponibilizados após publicação de matérias jornalísticas no Portal G1 e nas fanpages (Facebook), ambos relativos aos casos selecionados. Com a Análise de Conteúdo dos posts, identificamos e categorizamos a fala do consumidor contemporâneo, sendo assim possível comprovar que as organizações/marcas se valem da cultura do massivo, não dialogando com seus consumidores, pois utilizam as redes sociais on-line ainda de forma unidirecional, além de não darem a devida atenção ao atual fluxo onde se evidencia a opinião compartilhada dos consumidores da sociedade em rede.

Slow cycling of unphosphorylated myosin is inhibited by calponin, thus keeping smooth muscle relaxed

A key unanswered question in smooth muscle biology is whether phosphorylation of the myosin regulatory light chain (RLC) is sufficient for regulation of contraction, or if thin-filament-based regulatory systems also contribute to this process. To address this issue, the endogenous RLC was extracted from single smooth muscle cells and replaced with either a thiophosphorylated RLC or a mutant RLC (T18A/S19A) that cannot be phosphorylated by myosin light chain kinase. The actin-binding protein calponin was also extracted. Following photolysis of caged ATP, cells without calponin that contained a nonphosphorylatable RLC shortened at 30% of the velocity and produced 65% of the isometric force of cells reconstituted with the thiophosphorylated RLC. The contraction of cells reconstituted with nonphosphorylatable RLC was, however, specifically suppressed in cells that contained calponin. These results indicate that calponin is required to maintain cells in a relaxed state, and that in the absence of this inhibition, dephosphorylated cross-bridges can slowly cycle and generate force. These findings thus provide a possible framework for understanding the development of latch contraction, a widely studied but poorly understood feature of smooth muscle.

Homeostatic expansion and phenotypic conversion of naïve T cells in response to self peptide/MHC ligands

Recent data suggest that survival of resting, naïve T cells requires an interaction with self MHC molecules. From analysis of the class I MHC-restricted T cell receptor transgenic strain OT-I, we report a different response. Rather than merely surviving, these T cells proliferated slowly after transfer into T-depleted syngeneic hosts. This expansion required both T cell “space” and expression of normal levels of self class I MHC molecules. Furthermore, we demonstrate that during homeostatic expansion in a suitable environment, naïve phenotype (CD44low) OT-I T cells converted to memory phenotype (CD44med/high), despite the absence of foreign antigenic stimulation. On the other hand, cells undergoing homeostatic expansion did not acquire cytolytic effector function. The significance of these data for reactivity of T cells with self peptide/MHC ligands and the implications for normal and abnormal T cell homeostasis are discussed.

Amino Acid Sequence Requirements of the Transmembrane and Cytoplasmic Domains of Influenza Virus Hemagglutinin for Viable Membrane Fusion

The amino acid sequence requirements of the transmembrane (TM) domain and cytoplasmic tail (CT) of the hemagglutinin (HA) of influenza virus in membrane fusion have been investigated. Fusion properties of wild-type HA were compared with those of chimeras consisting of the ectodomain of HA and the TM domain and/or CT of polyimmunoglobulin receptor, a nonviral integral membrane protein. The presence of a CT was not required for fusion. But when a TM domain and CT were present, fusion activity was greater when they were derived from the same protein than derived from different proteins. In fact, the chimera with a TM domain of HA and truncated CT of polyimmunoglobulin receptor did not support full fusion, indicating that the two regions are not functionally independent. Despite the fact that there is wide latitude in the sequence of the TM domain that supports fusion, a point mutation of a semiconserved residue within the TM domain of HA inhibited fusion. The ability of a foreign TM domain to support fusion contradicts the hypothesis that a pore is composed solely of fusion proteins and supports the theory that the TM domain creates fusion pores after a stage of hemifusion has been achieved.

A Specific Point Mutant at Position 1 of the Influenza Hemagglutinin Fusion Peptide Displays a Hemifusion Phenotype

We showed previously that substitution of the first residue of the influenza hemagglutinin (HA) fusion peptide Gly1 with Glu abolishes fusion activity. In the present study we asked whether this striking phenotype was due to the charge or side-chain volume of the substituted Glu. To do this we generated and characterized six mutants with substitutions at position 1: Gly1 to Ala, Ser, Val, Glu, Gln, or Lys. We found the following. All mutants were expressed at the cell surface, could be cleaved from the precursor (HA0) to the fusion permissive form (HA1-S-S-HA2), bound antibodies against the major antigenic site, bound red blood cells, and changed conformation at low pH. Only Gly, Ala, and Ser supported lipid mixing during fusion with red blood cells. Only Gly and Ala supported content mixing. Ser HA, therefore, displayed a hemifusion phenotype. The hemifusion phenotype of Ser HA was confirmed by electrophysiological studies. Our findings indicate that the first residue of the HA fusion peptide must be small (e.g., Gly, Ala, or Ser) to promote lipid mixing and must be small and apolar (e.g., Gly or Ala) to support both lipid and content mixing. The finding that Val HA displays no fusion activity underscores the idea that hydrophobicity is not the sole factor dictating fusion peptide function. The surprising finding that Ser HA displays hemifusion suggests that the HA ectodomain functions not only in the first stage of fusion, lipid mixing, but also, either directly or indirectly, in the second stage of fusion, content mixing.

Resveratrol, a polyphenolic compound found in grapes and wine, is an agonist for the estrogen receptor

The phytochemical resveratrol, which is found in grapes and wine, has been reported to have a variety of anti-inflammatory, anti-platelet, and anti-carcinogenic effects. Based on its structural similarity to diethylstilbestrol, a synthetic estrogen, we examined whether resveratrol might be a phytoestrogen. At concentrations (≈3–10 μM) comparable to those required for its other biological effects, resveratrol inhibited the binding of labeled estradiol to the estrogen receptor and it activated transcription of estrogen-responsive reporter genes transfected into human breast cancer cells. This transcriptional activation was estrogen receptor-dependent, required an estrogen response element in the reporter gene, and was inhibited by specific estrogen antagonists. In some cell types (e.g., MCF-7 cells), resveratrol functioned as a superagonist (i.e., produced a greater maximal transcriptional response than estradiol) whereas in others it produced activation equal to or less than that of estradiol. Resveratrol also increased the expression of native estrogen-regulated genes, and it stimulated the proliferation of estrogen-dependent T47D breast cancer cells. We conclude that resveratrol is a phytoestrogen and that it exhibits variable degrees of estrogen receptor agonism in different test systems. The estrogenic actions of resveratrol broaden the spectrum of its biological actions and may be relevant to the reported cardiovascular benefits of drinking wine.

An unliganded thyroid hormone receptor causes severe neurological dysfunction

Congenital hypothyroidism and the thyroid hormone (T3) resistance syndrome are associated with severe central nervous system (CNS) dysfunction. Because thyroid hormones are thought to act principally by binding to their nuclear receptors (TRs), it is unexplained why TR knock-out animals are reported to have normal CNS structure and function. To investigate this discrepancy further, a T3 binding mutation was introduced into the mouse TR-β locus by homologous recombination. Because of this T3 binding defect, the mutant TR constitutively interacts with corepressor proteins and mimics the hypothyroid state, regardless of the circulating thyroid hormone concentrations. Severe abnormalities in cerebellar development and function and abnormal hippocampal gene expression and learning were found. These findings demonstrate the specific and deleterious action of unliganded TR in the brain and suggest the importance of corepressors bound to TR in the pathogenesis of hypothyroidism.

A quantitative model for membrane fusion based on low-energy intermediates

The energetics of a fusion pathway is considered, starting from the contact site where two apposed membranes each locally protrude (as “nipples”) toward each other. The equilibrium distance between the tips of the two nipples is determined by a balance of physical forces: repulsion caused by hydration and attraction generated by fusion proteins. The energy to create the initial stalk, caused by bending of cis monolayer leaflets, is much less when the stalk forms between nipples rather than parallel flat membranes. The stalk cannot, however, expand by bending deformations alone, because this would necessitate the creation of a hydrophobic void of prohibitively high energy. But small movements of the lipids out of the plane of their monolayers allow transformation of the stalk into a modified stalk. This intermediate, not previously considered, is a low-energy structure that can reconfigure into a fusion pore via an additional intermediate, the prepore. The lipids of this latter structure are oriented as in a fusion pore, but the bilayer is locally compressed. All membrane rearrangements occur in a discrete local region without creation of an extended hemifusion diaphragm. Importantly, all steps of the proposed pathway are energetically feasible.

Controlled Cytokinin Production in Transgenic Tobacco Using a Copper-Inducible Promoter

The cytokinin group of plant hormones regulates aspects of plant growth and development, including the release of lateral buds from apical dominance and the delay of senescence. In this work the native promoter of a cytokinin synthase gene (ipt) was removed and replaced with a Cu-controllable promoter. Tobacco (Nicotiana tabacum L. cv tabacum) transformed with this Cu-inducible ipt gene (Cu-ipt) was morphologically identical to controls under noninductive conditions in almost all lines produced. However, three lines grew in an altered state, which is indicative of cytokinin overproduction and was confirmed by a full cytokinin analysis of one of these lines. The in vitro treatment of morphologically normal Cu-ipt transformants with Cu2+ resulted in delayed leaf senescence and an increase in cytokinin concentration in the one line analyzed. In vivo, inductive conditions resulted in a significant release of lateral buds from apical dominance. The morphological changes seen during these experiments may reflect the spatial aspect of control exerted by this gene expression system, namely expression from the root tissue only. These results confirmed that endogenous cytokinin concentrations in tobacco transformants can be temporally and spatially controlled by the induction of ipt gene expression through the Cu-controllable gene-expression system.

Aromatase (Cyp19) expression is up-regulated by targeted disruption of Dax1

DAX-1 [dosage-sensitive sex reversal, adrenal hypoplasia congenita (AHC) critical region on the X chromosome, gene 1] is an orphan nuclear receptor that represses transcription by steroidogenic factor-1 (SF-1), a factor that regulates expression of multiple steroidogenic enzymes and other genes involved in reproduction. Mutations in the human DAX1 gene (also known as AHC) cause the X-linked syndrome AHC, a disorder that is associated with hypogonadotropic hypogonadism also. Characterization of Dax1-deficient male mice revealed primary testicular defects that included Leydig cell hyperplasia (LCH) and progressive degeneration of the germinal epithelium, leading to infertility. In this study, we investigated the effect of Dax1 disruption on the expression profile of various steroidogenic enzyme genes in Leydig cells isolated from Dax1-deficient male mice. Expression of the aromatase (Cyp19) gene, which encodes the enzyme that converts testosterone to estradiol, was increased significantly in the Leydig cells isolated from mutant mice, whereas the expression of other proteins (e.g., StAR and Cyp11a) was not altered. In in vitro transfection studies, DAX-1 repressed the SF-1-mediated transactivation of the Cyp19 promoter but did not inhibit the StAR or Cyp11a promoters. Elevated Cyp19 expression was accompanied by increased intratesticular levels of estradiol. Administration of tamoxifen, a selective estrogen-receptor modulator, restored fertility to the Dax1-deficient male mice and partially corrected LCH, suggesting that estrogen excess contributes to LCH and infertility. Based on these in vivo and in vitro analyses, aromatase seems to be a physiologic target of Dax-1 in Leydig cells, and increased Cyp19 expression may account, in part, for the infertility and LCH in Dax1-deficient mice.

Thyroid hormone (T3) inhibits ciprofibrate-induced transcription of genes encoding beta-oxidation enzymes: cross talk between peroxisome proliferator and T3 signaling pathways.

Peroxisome proliferators cause rapid and coordinated transcriptional activation of genes encoding peroxisomal beta-oxidation system enzymes by activating peroxisome proliferator-activated receptor (PPAR) isoform(s). Since the thyroid hormone (T3; 3,3',5-triiodothyronine) receptor (TR), another member of the nuclear hormone receptor superfamily, regulates a subset of fatty acid metabolism genes shared with PPAR, we examined the possibility of interplay between peroxisome proliferator and T3 signaling pathways. T3 inhibited ciprofibrate-induced luciferase activity as well as the endogenous peroxisomal beta-oxidation enzymes in transgenic mice carrying a 3.2-kb 5'-flanking region of the rat peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase gene fused to the coding region of luciferase. Transfection assays in hepatoma H4-II-E-C3 and CV-1 cells indicated that this inhibition is mediated by TR in a ligand-dependent fashion. Gel shift assays revealed that modulation of PPAR action by TR occurs through titration of limiting amounts of retinoid X receptor (RXR) required for PPAR activation. Increasing amounts of RXR partially reversed the inhibition in a reciprocal manner; PPAR also inhibited TR activation. Results with heterodimerization-deficient TR and PPAR mutants further confirmed that interaction between PPAR and TR signaling systems is indirect. These results suggest that a convergence of the peroxisome proliferator and T3 signaling pathways occurs through their common interaction with the heterodimeric partner RXR.