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The manufacture of madness: A comparative study of the by Thomas Stephen Szasz

By Thomas Stephen Szasz

During this seminal paintings, Dr. Szasz examines the similarities among the Inquisition and institutional psychiatry. His function is to teach "that the assumption in psychological affliction and the social activities to which it leads have an identical ethical implications and political outcomes as had the idea in witchcraft and the social activities to which it led."

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B. (1992). 7Å of the bovine papillomavirus-1 E2 DNA-binding protein bound to its DNA target. Nature, 359, 505–512. , Camiolo, S. , & Yates, J. L. (1993). Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection. EMBO Journal, 12, 4933–4944. Jones, C. , Hayward, S. , & Rawlins, D. R. (1989). Interaction of the lymphocyte-derived Epstein-Barr virus nuclear antigen EBNA-1 with its DNA-binding sites. Journal of Virology, 63, 101–110.

2012a). Consistent with these p53 effects, the presence of EBNA1 in all of these cell lines resulted in decreased apoptosis after DNA damage, although this may not be entirely due to the lowered p53 levels. As discussed below, EBNA1 also induces the loss of PML nuclear bodies which are important for apoptosis, in part because they facilitate the activation of p53 through acetylation. Therefore, EBNA1 likely inhibits p53 function in multiple ways (at least in epithelial cells) thereby promoting cell survival.

In addition, PML nuclear bodies are part of the innate immune response and act to suppress productive infections of several viruses through inhibition of viral gene expression and replication (Everett and Chelbi-Alix 2007; Geoffroy and Chelbi-Alix 2011; Reichelt et al. 2011). PML proteins, which are comprised of six nuclear isoforms, interact with each other to form the structural basis of the PML nuclear body with which many additional proteins then interact. To counteract the inhibition of viral infection by PML nuclear bodies, many viruses encode proteins that disrupt them, either by inducing the degradation of the PML proteins or by interfering with the interactions of PML proteins to form the bodies (Everett 2001).

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