Borges, Cortázar, el galache y la gurupa sureña. Apostilla al debate sobre el (anti)hispanismo en Argentina

Una historia del Hispanismo en Argentina no estaría completa, tal como ha demostrado José Luis de Diego, sin la larga serie de manifes¬taciones antiespañolas que se registraron desde el siglo XIX hasta el presente. Entre los numerosos integrantes de la lista de reconocidos intelectuales que polemizaron con la antigua metrópolis, se encuentra Julio Cortázar, quien en distintos momentos de su carrera expresó a través de la ficción sus divergencias con una estética y una forma de concebir la literatura caducas que identificaba con España. Alentando el propósito de mantener vivo el debate sobre el tema iniciado en el número 5 de Olivar, la siguiente nota desmonta las operaciones que lleva a cabo el autor de en un capítulo de Un tal Lucas análisis detenido del fragmento así como de las relaciones que tiende hacia otras obras del mismo escritor, me ha permitido esbozar una hipótesis sobre la construcción del antihispanismo cortazariano.

Reflexión : punto de partida para la anti naturalización

Las cuestiones y doctrinas científicas estudiadas deben servir de instrumentos para el análisis y la reflexión, nunca constituir fines en sí mismos, ni doctrinas de salvación (no se adhiere a una teoría como a una religión). La lectura de Morgenthau o Aron, Rosencrance o Kaplan, Keohane o Kratochwill por citar algunos, debe permitir "ver" mejor, ya sea aspectos de la práctica científica, ya sean sus dimensiones éticas o políticas. Ello porque pasa de las cuestiones epistemológicas a las ético-políticas, y viceversa, casi sin solución de continuidad. El propósito de este artículo es reflexionar sobre ciertos supuestos que han naturalizado el conocimiento en las Relaciones Internacionales.

Anti-factualismo : En busca de un criterio de diferenciación

Fil: Díaz Legaspe, Justina. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina.

Borges, Cortázar, el galache y la gurupa sureña. Apostilla al debate sobre el (anti)hispanismo en Argentina

Una historia del Hispanismo en Argentina no estaría completa, tal como ha demostrado José Luis de Diego, sin la larga serie de manifes¬taciones antiespañolas que se registraron desde el siglo XIX hasta el presente. Entre los numerosos integrantes de la lista de reconocidos intelectuales que polemizaron con la antigua metrópolis, se encuentra Julio Cortázar, quien en distintos momentos de su carrera expresó a través de la ficción sus divergencias con una estética y una forma de concebir la literatura caducas que identificaba con España. Alentando el propósito de mantener vivo el debate sobre el tema iniciado en el número 5 de Olivar, la siguiente nota desmonta las operaciones que lleva a cabo el autor de en un capítulo de Un tal Lucas análisis detenido del fragmento así como de las relaciones que tiende hacia otras obras del mismo escritor, me ha permitido esbozar una hipótesis sobre la construcción del antihispanismo cortazariano.

Reflexión : punto de partida para la anti naturalización

Las cuestiones y doctrinas científicas estudiadas deben servir de instrumentos para el análisis y la reflexión, nunca constituir fines en sí mismos, ni doctrinas de salvación (no se adhiere a una teoría como a una religión). La lectura de Morgenthau o Aron, Rosencrance o Kaplan, Keohane o Kratochwill por citar algunos, debe permitir "ver" mejor, ya sea aspectos de la práctica científica, ya sean sus dimensiones éticas o políticas. Ello porque pasa de las cuestiones epistemológicas a las ético-políticas, y viceversa, casi sin solución de continuidad. El propósito de este artículo es reflexionar sobre ciertos supuestos que han naturalizado el conocimiento en las Relaciones Internacionales.

Direct adenovirus-mediated gene transfer of interleukin 1 and tumor necrosis factor α soluble receptors to rabbit knees with experimental arthritis has local and distal anti-arthritic effects

Adenoviral vectors were used to deliver genes encoding a soluble interleukin 1 (IL-1)-type I receptor-IgG fusion protein and/or a soluble type I tumor necrosis factor α (TNFα) receptor-IgG fusion protein directly to the knees of rabbits with antigen-induced arthritis. When tested individually, knees receiving the soluble IL-1 receptor had significantly reduced cartilage matrix degradation and white blood cell infiltration into the joint space. Delivery of the soluble TNFα receptor was less effective, having only a moderate effect on white blood cell infiltration and no effect on cartilage breakdown. When both soluble receptors were used together, there was a greater inhibition of white blood cell infiltration and cartilage breakdown with a considerable reduction of synovitis. Interestingly, anti-arthritic effects were also seen in contralateral control knees receiving only a marker gene, suggesting that sustained local inhibition of disease activity in one joint may confer an anti-arthritic effect on other joints. These results suggest that local intra-articular gene transfer could be used to treat systemic polyarticular arthritides.

CTLA4-Ig and anti-CD40 ligand prevent renal allograft rejection in primates

Selective inhibition of T cell costimulation using the B7-specific fusion protein CTLA4-Ig has been shown to induce long-term allograft survival in rodents. Antibodies preventing the interaction between CD40 and its T cell-based ligand CD154 (CD40L) have been shown in rodents to act synergistically with CTLA4-Ig. It has thus been hypothesized that these agents might be capable of inducing long-term acceptance of allografted tissues in primates. To test this hypothesis in a relevant preclinical model, CTLA4-Ig and the CD40L-specific monoclonal antibody 5C8 were tested in rhesus monkeys. Both agents effectively inhibited rhesus mixed lymphocyte reactions, but the combination was 100 times more effective than either drug alone. Renal allografts were transplanted into nephectomized rhesus monkeys shown to be disparate at major histocompatibility complex class I and class II loci. Control animals rejected in 5–8 days. Brief induction doses of CTLA4-Ig or 5C8 alone significantly prolonged rejection-free survival (20–98 days). Two of four animals treated with both agents experienced extended (>150 days) rejection-free allograft survival. Two animals treated with 5C8 alone and one animal treated with both 5C8 and CTLA4-Ig experienced late, biopsy-proven rejection, but a repeat course of their induction regimen successfully restored normal graft function. Neither drug affected peripheral T cell or B cell counts. There were no clinically evident side effects or rejections during treatment. We conclude that CTLA4-Ig and 5C8 can both prevent and reverse acute allograft rejection, significantly prolonging the survival of major histocompatibility complex-mismatched renal allografts in primates without the need for chronic immunosuppression.

Inhibition of interferon γ induced interleukin 12 production: A potential mechanism for the anti-inflammatory activities of tumor necrosis factor

Inflammation is associated with production of cytokines and chemokines that recruit and activate inflammatory cells. Interleukin (IL) 12 produced by macrophages in response to various stimuli is a potent inducer of interferon (IFN) γ production. IFN-γ, in turn, markedly enhances IL-12 production. Although the immune response is typically self-limiting, the mechanisms involved are unclear. We demonstrate that IFN-γ inhibits production of chemokines (macrophage inflammatory proteins MIP-1α and MIP-1β). Furthermore, pre-exposure to tumor necrosis factor (TNF) inhibited IFN-γ priming for production of high levels of IL-12 by macrophages in vitro. Inhibition of IL-12 by TNF can be mediated by both IL-10-dependent and IL-10-independent mechanisms. To determine whether TNF inhibition of IFN-γ-induced IL-12 production contributed to the resolution of an inflammatory response in vivo, the response of TNF+/+ and TNF−/− mice injected with Corynebacterium parvum were compared. TNF−/− mice developed a delayed, but vigorous, inflammatory response leading to death, whereas TNF+/+ mice exhibited a prompt response that resolved. Serum IL-12 levels were elevated 3-fold in C. parvum-treated TNF−/− mice compared with TNF+/+ mice. Treatment with a neutralizing anti-IL-12 antibody led to resolution of the response to C. parvum in TNF−/− mice. We conclude that the role of TNF in limiting the extent and duration of inflammatory responses in vivo involves its capacity to regulate macrophage IL-12 production. IFN-γ inhibition of chemokine production and inhibition of IFN-γ-induced IL-12 production by TNF provide potential mechanisms by which these cytokines can exert anti-inflammatory/repair function(s).

Enhanced tyrosine phosphorylation of the 2B subunit of the N-methyl-D-aspartate receptor in long-term potentiation.

Both serine/threonine and tyrosine phosphorylation of receptor proteins have been implicated in the process of long-term potentiation (LTP), but there has been no direct demonstration of a change in receptor phosphorylation after LTP induction. We show that, after induction of LTP in the dentate gyrus of anesthetized adult rats, there is an increase in the tyrosine phosphorylation of the 2B subunit of the N-methyl-D-aspartate (NMDA) receptor (NR2B), as well as several other unidentified proteins. Tyrosine phosphorylation of NR2B was measured in two ways: binding of antiphosphotyrosine antibodies (PY20) to glycoprotein(s) of 180 kDa (GP180) purified on Con A-Sepharose and binding of anti-NR2B antibodies to tyrosine-phosphorylated proteins purified on PY20-agarose. Three hours after LTP induction, anti-NR2B binding to tyrosine phosphorylated proteins, expressed as a ratio of tetanized to control dentate (Tet/Con), was 2.21 +/- 0.50 and PY20 binding to GP180 was 1.68 +/- 0.16. This increase in the number of tyrosine phosphorylated NR2B subunits occurred without a change in the total number of NR2B subunits. When the induction of LTP was blocked by pretreatment of the animal with the NMDA receptor antagonist MK801, the increase in PY20 binding to GP180 was also blocked (Tet/Con = 1.09 +/- 0.26). The increased PY20 binding to GP180 was also apparent 15 min after LTP induction (Tet/Con = 1.41 +/- 0.16) but not detectable 5 min after LTP induction (Tet/Con = 1.01 +/- 0.19). These results suggest that tyrosine phosphorylation of the NMDA receptor contributes to the maintenance of LTP.

In vivo tissue distribution of CD4 lymphocytes in mice determined by radioimmunoscintigraphy with an 111In-labeled anti-CD4 monoclonal antibody.

The tissue distribution of CD4 lymphocytes in normal C57/BL mice and CD4 knockout mice was determined by biodistribution measurements and gamma camera imaging with an 111In-labeled rat IgG2b monoclonal antibody directed against the murine CD-4 antigen. In normal mice high concentrations of antibody accumulated in the spleen and lymph nodes. At 45 hr after injection, the concentration of radiolabel in the spleen and lymph nodes of normal mice were 10- to 20-fold greater than in the corresponding tissue of the CD4 knockout mice and nonlymphoid tissues of both types of mice. At 24 and 45 hr, gamma camera images showed high concentrations of radiolabeled antibody in lymph node and spleen of normal but not knockout mice. These results indicate that radioimmunoscintigraphy with 111In-anti-CD4 is an excellent method for studying tissue distribution of CD lymphocytes in mice. Using an equivalent anti-human CD antibody, this method might be useful for studying the pathophysiology of conditions in which these cells play a critical role and for monitoring therapies for these disorders.