Reverse the Curse: Colonialist Legacies of the Magic Poem

This dissertation investigates the conceptual relationships between poetry, magic, and race and their effects on both intellectual and creative practices from modernism through the post-war era. In doing so, this study works cross-disciplinarily, tracing early anthropological and sociological characterizations of primitive religion in connection to early-to-mid-twentieth-century literary study and writing. In working across disciplines at this particularly fungible moment in the history of the academy, this dissertation attempts to understand how the concurrent colonial global context effects the production and organization of knowledge just prior to and during modernism. It ultimately seeks to de-colonize literary thinking about poetry by performing a racial critique of the role of magical thinking in its generic conception and production. The first chapter establishes the intellectual history of the dissertation’s key problem, the presence of primitivism throughout modernist and post-modernish approaches to poetry and the desire for this poetry to offer reparation; examines the ethnographic texts, especially Marcel Mauss’s General Theory of Magic, that relate poetic language to the language of magic ritual and animistic belief systems; considers how these foundational beliefs continued to influence modernist critics like Theodor Adorno and C.L.R. James, and how certain poets and critics attempt to subvert these intellectual trends that associate blackness with magic and magic with poetry; and lastly questions the ethical implications of assuming that poetry’s “magic” could cure socio-cultural loss. The second and third chapters further develop and test the dissertation’s argument that regardless of poets’ intentions, magic operates within their understanding of poetic function, and that these understandings stem from racist, colonialist understandings of primitive space, time, and culture, while simultaneously attempting to understand their works’ attitude toward poetic reparation. In the second chapter, I examine Gertrude Stein’s 1932 Stanzas in Meditation in an attempt to understand the text’s relationship to concepts of magical language, and its trance-like, reparative effect on readers, an effect complicated by its appropriation of primitivist concepts of time. In the final chapter, I turn to Amiri Baraka’s 1969 compilation Black Magic to explore this work’s relationship to its titular “magic.” I ultimately demonstrate how Baraka’s work re-theorizes a kind of poetic spirituality that eschews white capitalist magic and offers a materialist, pragmatic poetics for surviving racism and strengthening Black consciousness. In concluding, I look to the contemporary moment and claim that the current upswing in the poetry community’s interest in the occult serves as further evidence for one, how the role of magic and poetry corresponds to a social desire for reparation, and, two, how the racialized thinking at stake in the invocation of magic in poetry continues to merit critical and popular examination

Activating Mutations of RRAS2 Are a Rare Cause of Noonan Syndrome

Aberrant signaling through pathways controlling cell response to extracellular stimuli constitutes a central theme in disorders affecting development. Signaling through RAS and the MAPK cascade controls a variety of cell decisions in response to cytokines, hormones, and growth factors, and its upregulation causes Noonan syndrome (NS), a developmental disorder whose major features include a distinctive facies, a wide spectrum of cardiac defects, short stature, variable cognitive impairment, and predisposition to malignancies. NS is genetically heterogeneous, and mutations in more than ten genes have been reported to underlie this disorder. Despite the large number of genes implicated, about 10%-20% of affected individuals with a clinical diagnosis of NS do not have mutations in known RASopathy-associated genes, indicating that additional unidentified genes contribute to the disease, when mutated. By using a mixed strategy of functional candidacy and exome sequencing, we identify RRAS2 as a gene implicated in NS in six unrelated subjects/families. We show that the NS-causing RRAS2 variants affect highly conserved residues localized around the nucleotide binding pocket of the GTPase and are predicted to variably affect diverse aspects of RRAS2 biochemical behavior, including nucleotide binding, GTP hydrolysis, and interaction with effectors. Additionally, all pathogenic variants increase activation of the MAPK cascade and variably impact cell morphology and cytoskeletal rearrangement. Finally, we provide a characterization of the clinical phenotype associated with RRAS2 mutations

Deficiency for the ubiquitin ligase ube3b in a blepharophimosis-ptosis- intellectual-disability syndrome

Ubiquitination plays a crucial role in neurodevelopment as exemplified by Angelman syndrome, which is caused by genetic alterations of the ubiquitin ligase-encoding UBE3A gene. Although the function of UBE3A has been widely studied, little is known about its paralog UBE3B. By using exome and capillary sequencing, we here identify biallelic UBE3B mutations in four patients from three unrelated families presenting an autosomal-recessive blepharophimosis- ptosis-intellectual-disability syndrome characterized by developmental delay, growth retardation with a small head circumference, facial dysmorphisms, and low cholesterol levels. UBE3B encodes an uncharacterized E3 ubiquitin ligase. The identified UBE3B variants include one frameshift and two splice-site mutations as well as a missense substitution affecting the highly conserved HECT domain. Disruption of mouse Ube3b leads to reduced viability and recapitulates key aspects of the human disorder, such as reduced weight and brain size and a downregulation of cholesterol synthesis. We establish that the probable Caenorhabditis elegans ortholog of UBE3B, oxi-1, functions in the ubiquitin/proteasome system in vivo and is especially required under oxidative stress conditions. Our data reveal the pleiotropic effects of UBE3B deficiency and reinforce the physiological importance of ubiquitination in neuronal development and function in mammals. © 2012 The American Society of Human Genetics.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Immunovirological parameters and cytokines in HIV infection

Although modern combined antiretroviral therapies (cART) result in lower morbidity and mortality and a visible improvement of clinical and laboratory parameters in HIV-infected, it is known that their long-term use contributes to appearance of the many events unrelated to AIDS such as cardiovascular diseases, cancer and osteoporosis, comorbidities which have been proposed as some of the most important that deprive the majority of infected to present an even better prognosis. This is because even with a decrease in inflammation and immune activation after drug intervention to the patient, these parameters remain higher than those shown by healthy individuals and the imbalance of cytokine profiles also persists. Therefore, evaluations of other biomarkers in clinical practice are needed to complement the exams already carried out routinely and allow more effective monitoring of HIV patients. This review aims to investigate the role of cytokines as potential markers showing studies on their behavior in various stages of HIV infection, with or without cART