Cockney, pseudo-slang et argot de série noire : San-Antonio et le moment Peter Cheyney du roman noir français

This article examines how in post-war France slang became a byword for the noir genre. It considers the mechanisms, models, networks and translators' practices which set the tone for the "Série Noire”, whose influence, both written and on the screen, had, within a decade, become, a "mythology" studied by Roland Barthes. It argues that this use of slang is redolent of the inauthenticity which characterises this stage in the reception of the Noir genre in France. It is certain that this artificial French slang is far from devoid of charm, or even mystery. But it tends to depreciate and deform the translated works and seems to be the hallmark of an era that might have defined and acclimatised Noir fiction in France, yet remains one which has not fully understood the gravity of its purpose. While such translations seem outdated nowadays (if not quite incomprehensible ), original works written at the time in French by writers inspired by the model of " pseudo- slang" and the fashionability of American popular culture have benefited from them. In this very inauthenticity, derivative novels have found a licence for invention and freedom, with authors such as Cocteau hailing it as a revival of the French written language. We see here how the adventures of Commissaire San Antonio, by Frédéric Dard constitute the best examples of this new creativity in French and draw upon a template set for the reception of American literature

Selective induction of apoptosis by the pyrrolo-1,5-benzoxazepine 7-[[dimethylcarbamoyl]oxy]-6-(2-naphthyl)pyrrolo-[2,1-d] (1,5)-benzoxazepine (PBOX-6) in Leukemia cells occurs via the c-Jun NH2-terminal kinase-dependent phosphorylation and inactivation of Bcl-2 and Bcl-XL

Overexpression of the Bcl-2 proto-oncogene in tumor cells confers resistance against chemotherapeutic drugs. In this study, we describe how the novel pyrrolo-1,5-benzoxazepine compound 7-[[dimethylcarbamoyl]oxy]-6-(2-naphthyl)pyrrolo-[2,1-d] (1,5)-benzoxazepine (PBOX-6) selectively induces apoptosis in Bcl-2-overexpressing cancer cells, whereas it shows no cytotoxic effect on normal peripheral blood mononuclear cells. PBOX-6 overcomes Bcl-2-mediated resistance to apoptosis in chronic myelogenous leukemia (CML) K562 cells by the time- and dose-dependent phosphorylation and inactivation of antiapoptotic Bcl-2 family members Bcl-2 and Bcl-XL. PBOX-6 also induces Bcl-2 phosphorylation and apoptosis in wild-type T leukemia CEM cells and cells overexpressing Bcl-2. This is in contrast to chemotherapeutic agents such as etoposide, actinomycin D, and ultraviolet irradiation, whereby overexpression of Bcl-2 confers resistance against apoptosis. In addition, PBOX-6 induces Bcl-2 phosphorylation and apoptosis in wild-type Jurkat acute lymphoblastic leukemia cells and cells overexpressing Bcl-2. However, Jurkat cells containing a Bcl-2 triple mutant, whereby the principal Bcl-2 phosphorylation sites are mutated to alanine, demonstrate resistance against Bcl-2 phosphorylation and apoptosis. PBOX-6 also induces the early and transient activation of c-Jun NH2-terminal kinase (JNK) in CEM cells. Inhibition of JNK activity prevents Bcl-2 phosphorylation and apoptosis, implicating JNK in the upstream signaling pathway leading to Bcl-2 phosphorylation. Collectively, these findings identify Bcl-2 phosphorylation and inactivation as a critical step in the apoptotic pathway induced by PBOX-6 and highlight its potential as an effective antileukemic agent.

Activation of the c-Jun N-terminal kinase (JNK) signaling pathway is essential during PBOX-6-induced apoptosis in chronic myelogenous leukemia (CML) cells

The mitogen-activated protein (MAP) kinase family is activated in response to a wide variety of external stress signals such as UV irradiation, heat shock, and many chemotherapeutic drugs and leads to the induction of apoptosis. A novel series of pyrrolo-1,5-benzoxazepines have been shown to potently induce apoptosis in chronic myelogenous leukemia (CML) cells, which are resistant to many chemotherapeutic agents. In this study we have delineated part of the mechanism by which a representative compound known as PBOX-6 induces apoptosis. We have investigated whether PBOX-6 induces activation of MAP kinase signaling pathways in CML cells. Treatment of K562 cells with PBOX-6 resulted in the transient activation of two JNK isoforms, JNK1 and JNK2. In contrast, PBOX-6 did not activate the extracellular signal-regulated kinase (ERK) or p38. Apoptosis was found to occur independently of the small GTPases Ras, Rac, and Cdc42 but involved phosphorylation of the JNK substrates, c-Jun and ATF-2. Pretreatment of K562 cells with the JNK inhibitor, dicoumarol, abolished PBOX-6-induced phosphorylation of c-Jun and ATF-2 and inhibited the induced apoptosis, suggesting that JNK activation is an essential component of the apoptotic pathway induced by PBOX-6. Consistent with this finding, transfection of K562 cells with the JNK scaffold protein, JIP-1, inhibited JNK activity and apoptosis induced by PBOX-6. JIP-1 specifically scaffolds JNK, MKK7, and members of the mixed-lineage kinase (MLK) family, implicating these kinases upstream of JNK in the apoptotic pathway induced by PBOX-6 in K562 cells.

Proyecto de Factibilidad para la creación de una empresa dedicada a la elaboración de papel a base del pinzote de banano, ubicado en el sector Rumicucho, parroquia San Antonio de Pichincha, Canctón Quito. Provincia de Pichincha.

El presente trabajo investigativo contiene cinco capítulos los cuales están ordenados en una forma secuencial y lógica para el entendimiento de los lectores. El Capítulo I, es el Estudio de Mercado, en el cual como método de investigación se utilizo la encuesta, para conocer la cantidad de personas que requieren adquirí el producto, sus necesidades, además de indagar en las ofertas existentes, las tendencias que tienen estos, para de esta manera saber en qué mercado queremos incursionar y cuál sería la oferta que podemos presentar. El Capítulo II, es el Estudio de Tamaño y Localización, se analizo factores de producción, maquinaria los que permiten conocer cuál es el tamaño óptimo de la planta, el tamaño de la maquinaria para de esta manera analizar la distribución espacial de la planta. La localización a pesar de conocerla, se analizó para saber las características con las que cuenta este lugar tanto como las falencias del mismo. El Capítulo III, es el Estudio de Ingeniería del Proyecto, este nos permitió conocer los recursos humanos, de infraestructura, materia prima, de equipos y maquinaria, que se necesitarán para la implementación de la planta, el costo que estos implican, para considerar la selección adecuada de los mismos. El Capítulo VI, Estudio Financiero, es el que permite establecer la factibilidad del proyecto de manera cuantitativa a través de la inversión que se realizará, los, costos, los ingresos, que permiten conocer la utilidad que genera el proyecto, además de analizar con métodos financieros la viabilidad de la empresa a base de sus resultados. El Capítulo V, Análisis Legal y Organizacional, establece las bases jurídicas tanto internas y externas que debe cumplir la empresa, desde su constitución y durante todo el horizonte del proyecto. En lo referente a la organización se estable la misión, visión, organigramas y la importancia del personal en la empresa.

Chiapas a través de los viajeros del siglo XVII: aspectos narrativos e historia descriptiva en Thomas Gage y Antonio Vázquez de Espinosa

Chiapas representó en el siglo XVII una región donde confluían los mitos, temores y fascinaciones de colonos y europeos. Al ser visitada por Thomas Gage en su travesía hacia Guatemala, es descrita en su Nuevo reconocimiento de las Indias Occidentales de modo muy distinto cuando el narrador, como es este caso, registra sus vivencias personales e, incluso, pasionales. Sólo la historiografía moderna podría explicarnos particulares pasajes en que el viajero es abordado súbitamente por una realidad que pasa desapercibida a otros viajeros con un programa muy claro de supervisión y registro de datos, como es el caso de Antonio Vázquez de Espinosa en su Descripción de la Nueva España. Si el historiógrafo describe puntualmente flora, fauna y geografía, el narrador huele, paladea y recorre con nosotros el laberinto de la tierra chiapaneca. El paisaje a través de la persona, con todos los cabos sueltos y apariciones inexplicables para quien se interna en lo desconocido, cobran, a la luz de investigaciones recientes acerca del contexto sociohistórico de Chiapas, un sentido cabal que no sólo nos ilustra, sino que nos interna y se nos interna.

Narrativement vôtre San-Antonio, ou, La fictivité racontée

Comme l'ont souligné certains critiques, un des aspects essentiels de l'écriture sanantonienne réside dans la mise en scène de l'acte de narration. Dans le but de comprendre l'évolution de l'oeuvre de San-Antonio, l'analyse de cette caractéristique, à travers un corpus de romans parus dans cinq décennies différentes, s'est avérée opportune. L'étude du paratexte réel, d'une part, et de la représentation fictive du paratexte, d'autre part, démontre que cette mise en scène de la narration s'est développée et complexifiée de 1950 à 1980. Par la suite, cette pratique est demeurée, mais a été utilisée avec moins d'emphase. Par ailleurs, l'exploration des possibilités paratextuelles menée par San-Antonio révèle en creux les nombreuses conventions littéraires qui reposent sur le paratexte. Enfin, la mise en évidence de la narration est une sorte de défi au pouvoir de la fiction: la magie du récit opère toujours malgré ces évidents bris du réalisme.

A peptide inhibitor of C-jun N-terminal kinase modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Hemorrhage and resuscitation (H/R) leads to phosphorylation of mitogen-activated stress kinases, an event that is associated with organ damage. Recently, a specific, cell-penetrating, protease-resistant inhibitory peptide of the mitogen-activated protein kinase c-JUN N-terminal kinase (JNK) was developed (D-JNKI-1). Here, using this peptide, we tested if inhibition of JNK protects against organ damage after H/R. Male Sprague-Dawley rats were treated with D-JNKI-1 (11 mg/kg, i.p.) or vehicle. Thirty minutes later, rats were hemorrhaged for 1 h to a MAP of 30 to 35 mmHg and then resuscitated with 60% of the shed blood and twice the shed blood volume as Ringer lactate. Tissues were harvested 2 h later. ANOVA with Tukey post hoc analysis or Kruskal-Wallis ANOVA on ranks, P < 0.05, was considered significant. c-JUN N-terminal kinase inhibition decreased serum alanine aminotransferase activity as a marker of liver injury by 70%, serum creatine kinase activity by 67%, and serum lactate dehydrogenase activity by 60% as compared with vehicle treatment. The histological tissue damage observed was blunted after D-JNKI-1 pretreatment both for necrotic and apoptotic cell death. Hepatic leukocyte infiltration and serum IL-6 levels were largely diminished after D-JNKI-1 pretreatment. The extent of oxidative stress as evaluated by immunohistochemical detection of 4-hydroxynonenal was largely abrogated after JNK inhibition. After JNK inhibition, activation of cJUN after H/R was also reduced. Hemorrhage and resuscitation induces a systemic inflammatory response and leads to end-organ damage. These changes are mediated, at least in part, by JNK. Therefore, JNK inhibition deserves further evaluation as a potential treatment option in patients after resuscitated blood loss.