On Victor Li’s \u3cem\u3eThe Neo-Primitivist Turn: Critical Reflections on Alterity, Culture, and Modernity\u3c/em\u3e

The Neo-Primitivist Turn: Critical Reflections on Alterity, Culture, and Modernity (Victor Li

Facial diplegia with hyperreflexia-a mild Guillain-Barre Syndrome variant, to treat or not to treat?

Guillain Barre Syndrome (GBS) is readily diagnosed when the presentation is that of ascending weakness and areflexia. Atypical presentations with preserved, and at times, brisk reflexes, can be a diagnostic dilemma. We describe a patient with GBS who presented with facial diplegia and hyperreflexia on examination and discuss management options

Autophagy induction extends lifespan and reduces lipid content in response to frataxin silencing in C. elegans

Severe mitochondria deficiency leads to a number of devastating degenerative disorders, yet, mild mitochondrial dysfunction in different species, including the nematode Caenorhabditis elegans, can have pro-longevity effects. This apparent paradox indicates that cellular adaptation to partial mitochondrial stress can induce beneficial responses, but how this is achieved is largely unknown. Complete absence of frataxin, the mitochondrial protein defective in patients with Friedreich's ataxia, is lethal in C. elegans, while its partial deficiency extends animal lifespan in a p53 dependent manner. In this paper we provide further insight into frataxin control of C. elegans longevity by showing that a substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. We find that Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression. Reciprocally, frataxin expression modulates autophagy in the absence of p53. Human Friedreich ataxia-derived lymphoblasts also display increased autophagy, indicating an evolutionarily conserved response to reduced frataxin expression. In sum, we demonstrate a causal connection between induction of autophagy and lifespan extension following reduced frataxin expression, thus providing the rationale for investigating autophagy in the pathogenesis and treatment of Friedreich's ataxia and possibly other human mitochondria-associated disorders

The Victorian Newsletter (Spring 1987)

The Victorian Newsletter is sponsored for the Victorian Group of Modern Language Association by the Western Kentucky University and is published twice annually.Arnold among the Contentions of Criticism / Holly Laird -- Closure and the Victorian Novel, 1986 / Marianna Torgovnick -- Victorian Weaving: The Alienation of Work into Text in "The Lady of Shalott" / Gerhard Joseph -- The Tenant of Wildfell Hall: Anne Brontë's Jane Eyre / Margaret Mary Berg -- The Poor Fictionist' s Conscience: Point of View in the Palliser Novels / Patricia A. Vernon -- A New Perspective: Naturalism in George Moore's A Mummer's Wife / Judith Mitchell -- Browning's Testament of His Devisings in The Ring and the Book / Joseph A. Dupras -- Books Receive

Bisperoxovanadium, a phospho-tyrosine phosphatase inhibitor, reprograms myogenic cells to acquire a pluripotent, circulating phenotype

Satellite cells are the main source of myogenic progenitors in postnatal skeletal muscle, but their use in cell therapy for muscle disorders is limited because these cells cannot be delivered through circulation and they are rapidly exhausted in severe myopathies. The search for alternative donor cells is ongoing, but none of the candidates so far show all the features required for successful colonization and repair of diseased muscle. In this study, we show that bisperoxovanadium, a phospho-tyrosine phosphatase inhibitor, induces myogenic cells to acquire a gene expression profile and a differentiation potential consistent with the phenotype of a circulating precursors, while maintaining their myogenic potential. These effects are mediated, at least in part, by NF-kappa B activation through the Tyr42-I kappa B-alpha phosphorylation, as shown by the expression of the dominant negative mutant form of the p50 NF-kappa B subunit. Moreover, when bisperoxovanadium-treated cells are injected into the femoral artery of alpha-sarcoglican null dystrophic mice, they are able to circulate and to reach muscle tissue; importantly, they contribute to muscle regeneration, as shown by the expression of alpha-sarcoglican in some fibers. Our observations indicate that bisperoxovanadium, or similar compounds, may prove very valuable to obtain and to expand, from committed cells, multipotent cell populations suitable for gene-cell therapy applications and may help to understand the molecular basis of genome reprogramming and "stem-ness"

Hosts and hostages: Mass immigration and the power of hospitality in post-war British and Caribbean literature

This article examines the challenge to colonialist centre-periphery relations in post-war novels by white British and Caribbean writers. Concentrating on the relationship between political debates surrounding mass immigration and the marginalization of non-white migrants within British communities, I analyse texts that depict the threshold of the home as the politicized site of racial tension, namely Sam Selvon’s The Lonely Londoners (1956), V.S. Naipaul’s The Mimic Men (1967), Alan Sillitoe’s Saturday Night and Sunday Morning (1958), and Anthony Burgess’s The Right to an Answer (1960). In varying ways, these texts depict the durability of centre-periphery relations at local levels through the informal segregation of the colonizer and the colonized. In doing so they point to what Jacques Derrida has outlined, in Of Hospitality (2000), as the power relationship inherent in policies of immigration, whereby the host-nation remains in control of the conditions upon which hospitality rests

Active transcriptomic and proteomic reprogramming in the C-elegans nucleotide excision repair mutant xpa-1

Peer reviewe

The Homeobox Protein CEH-23 Mediates Prolonged Longevity in Response to Impaired Mitochondrial Electron Transport Chain in C. elegans

Recent findings indicate that perturbations of the mitochondrial electron transport chain (METC) can cause extended longevity in evolutionarily diverse organisms. To uncover the molecular basis of how altered METC increases lifespan in C. elegans, we performed an RNAi screen and revealed that three predicted transcription factors are specifically required for the extended longevity of mitochondrial mutants. In particular, we demonstrated that the nuclear homeobox protein CEH-23 uniquely mediates the longevity but not the slow development, reduced brood size, or resistance to oxidative stress associated with mitochondrial mutations. Furthermore, we showed that ceh-23 expression levels are responsive to altered METC, and enforced overexpression of ceh-23 is sufficient to extend lifespan in wild-type background. Our data point to mitochondria-to-nucleus communications to be key for longevity determination and highlight CEH-23 as a novel longevity factor capable of responding to mitochondrial perturbations. These findings provide a new paradigm for how mitochondria impact aging and age-dependent diseases