Sedução e feminilidade em transferência Seduction and femininity in transference

Buscam-se as relações entre a sedução e a transferência em psicanálise. Segue-se o desenvolvimento laplanchiano de que a transferência é provocada pelo analista, sendo essa provocação entendida ao modo de uma reativação da situação originária de sedução e passividade. Argumenta-se, então, sobre a facilitação, em psicanálise, do estabelecimento de circulação de fantasias da sexualidade "feminina", entendida também como originária. Discute-se, por fim, a presença da alteridade na relação transferencial em face da idéia, de Jacques André, do outro como o feminino.<br>This essay develops considerations on the relations between seduction and transference in psychoanalysis. Following Laplanche's suggestion, transference, in so far as it reactivates the originary situation of seduction and passivity, it is understood to be provoked by the analyst. Psychoanalysis is considered to facilitate the circulation of fantasies of "feminine" sexuality - also regarded as originary. The presence of alterity in transference is discussed from the point of view of J. André's comprehension of the other as feminine

Effect of Verapamil, an L-Type Calcium Channel Inhibitor, on Caveolin-3 Expression in Septic Mouse Hearts

Sepsis-induced myocardial dysfunction considerably increases mortality risk in patients with sepsis. Previous studies from our group have shown that sepsis alters the expression of structural proteins in cardiac cells, resulting in cardiomyocyte degeneration and impaired communication between cardiac cells. Caveolin-3 (CAV3) is a structural protein present in caveolae, located in the membrane of cardiac muscle cells, which regulates physiological processes such as calcium homeostasis. In sepsis, there is a disruption of calcium homeostasis, which increases the concentration of intracellular calcium, which can lead to the activation of potent cellular enzymes/proteases which cause severe cellular injury and death. The purpose of the present study was to test the hypotheses that sepsis induces CAV3 overexpression in the heart, and the regulation of L-type calcium channels directly relates to the regulation of CAV3 expression. Severe sepsis increases the expression of CAV3 in the heart, as immunostaining in our study showed CAV3 presence in the cardiomyocyte membrane and cytoplasm, in comparison with our control groups (without sepsis) that showed CAV3 presence predominantly in the plasma membrane. The administration of verapamil, an L-type calcium channel inhibitor, resulted in a decrease in mortality rates of septic mice. This effect was accompanied by a reduction in the expression of CAV3 and attenuation of cardiac lesions in septic mice treated with verapamil. Our results indicate that CAV3 has a vital role in cardiac dysfunction development in sepsis and that the regulation of L-type calcium channels may be related to its expression

Chemotherapeutic Potential of 17-AAG against Cutaneous Leishmaniasis Caused by <i>Leishmania (Viannia) braziliensis</i>

<div><p>Background</p><p>Leishmaniasis remains a worldwide public health problem. The limited therapeutic options, drug toxicity and reports of resistance, reinforce the need for the development of new treatment options. Previously, we showed that 17-(allylamino)-17-demethoxygeldanamycin (17-AAG), a Heat Shock Protein 90 (HSP90)-specific inhibitor, reduces <i>L. (L.) amazonensis</i> infection <i>in vitro</i>. Herein, we expand the current knowledge on the leishmanicidal activity of 17-AAG against cutaneous leishmaniasis, employing an experimental model of infection with <i>L. (V.) braziliensis</i>.</p><p>Methodology/Principal findings</p><p>Exposure of axenic <i>L. (V.) braziliensis</i> promastigotes to 17-AAG resulted in direct dose-dependent parasite killing. These results were extended to <i>L. (V.) braziliensis</i>-infected macrophages, an effect that was dissociated from the production of nitric oxide (NO), superoxide (O⁻²) or inflammatory mediators such as TNF-α, IL-6 and MCP-1. The leishmanicidal effect was then demonstrated <i>in vivo</i>, employing BALB/c mice infected with <i>L. braziliensis</i>. In this model, 17-AAG treatment resulted in smaller skin lesions and parasite counts were also significantly reduced. Lastly, 17-AAG showed a similar effect to amphotericin B regarding the ability to reduce parasite viability.</p><p>Conclusion/Significance</p><p>17-AAG effectively inhibited the growth of <i>L. braziliensis</i>, both <i>in vitro</i> and <i>in vivo</i>. Given the chronicity of <i>L. (V.) braziliensis</i> infection and its association with mucocutaneous leishmaniasis, 17-AAG can be envisaged as a new chemotherapeutic alternative for cutaneous Leishmaniasis.</p></div

Modulation of the mTOR Pathway by Curcumin in the Heart of Septic Mice

mTOR is a signaling pathway involved in cell survival, cell stress response, and protein synthesis that may be a key point in sepsis-induced cardiac dysfunction. Curcumin has been reported in vitro as an mTOR inhibitor compound; however, there are no studies demonstrating this effect in experimental sepsis. Thus, this study aimed to evaluate the action of curcumin on the mTOR pathway in the heart of septic mice. Free curcumin (FC) and nanocurcumin (NC) were used, and samples were obtained at 24 and 120 h after sepsis. Histopathological and ultrastructural analysis showed that treatments with FC and NC reduced cardiac lesions caused by sepsis. Our main results demonstrated that curcumin reduced mTORC1 and Raptor mRNA at 24 and 120 h compared with the septic group; in contrast, mTORC2 mRNA increased at 24 h. Additionally, the total mTOR mRNA expression was reduced at 24 h compared with the septic group. Our results indicate that treatment with curcumin and nanocurcumin promoted a cardioprotective response that could be related to the modulation of the mTOR pathway

17-AAG induces killing of <i>Leishmania (V.) braziliensis</i> promastigotes in a dose-dependent and irreversible manner.

<p><i>L. (V.) braziliensis</i> promastigotes were exposed to increasing concentrations of 17-AAG, to vehicle alone (DMSO) or were left unexposed (Lb) for 48 h. (A) The number of viable parasites was evaluated by direct counting. <i>L.(V) braziliensis</i> promastigotes were treated with 65 nM (IC₅₀) of 17-AAG for 24 h (B) and (C) 48 h. After washing, promastigotes were cultured for additional 48 h and the number of viable parasites was evaluated. Data, shown as mean ±SEM, are from one of two independent repeats (**<i>p</i><0.01 and ***<i>p</i><0.001).</p

<i>In vivo</i> treatment with 17-AAG decreases <i>L. (V.) braziliensis</i> infection.

<p>Mice were infected with <i>L. (V.) braziliensis</i> and four weeks later, mice were treated with 17-AAG, 3x a week for 3 weeks (boxed area) or with vehicle (DMSO) alone. (A) The course of lesion development was monitored weekly. (B) Disease burden [shown as Area Under the Curves (AUC) depicted in (A)] in mice treated with 17-AAG or injected with DMSO. Parasite load was determined at the infection site (C) and at the dLN (D), 6 weeks later, by limiting dilution analysis. Data, shown as mean ±SEM, are from one of two independent repeats, each performed with 10 mice in each group (**<i>p</i><0.01; *<i>p</i><0.05).</p