Raloxifene for improving attention and memory in schizophrenia?

Schizophrenia can affect people's thoughts, feelings, and behaviour, and it can be as if your brain was playing tricks on you.

BIFF to BAPFF: considering 'festival memory' in the face of innovation and change

As an art form, film has arguably always functioned as a stronghold for memory. Memories unfold in the stories told on screen, and remain preserved in the experiences of the audience viewing the film, at a particular time and place. The environment of a film festival further alters the viewing experience and its relationship to memory. The Brisbane International Film Festival (BIFF) was founded in 1992. After considerable disruption due to economic and socio-political changes, it took place for the last time in 2013. The change in BIFF’s leadership and programming agenda significantly impacted the festival’s image and its position on the wider festival circuit. Through an examination of cinema and memory) it will be argued that film festivals operate as (temporary) sites of memory, through the programming and screening of films, engagement with local audiences, and promotion of film culture. This specific and unique ‘festival memory’ inextricably links to the audience and the venue, and is curated by the festival programmers and staff, who carry a wealth of knowledge (not necessarily recorded), of past festivals, successes, and failures. The people involved, the festival staff and audience, act as caretakers of this ‘festival memory.’ This essay will therefore examine how the BIFF and its home, the Regent Theatre, have functioned as crucial ‘sites of memory’ for film and film culture in Brisbane, Australia.

Farewelling the regent: Considering 'festival memory' in the face of innovation and change

The rapid expansion of the international film festival circuit has included the loss of smaller, but well established festivals, often due to the perceived need for constant innovation and change. The Brisbane International Film Festival was founded in 1992. After considerable disruption to the festival’s leadership, programme and location due to economic and socio-political changes, it was held for the last time in 2013. Nafus and Anderson cite the term ‘lieux de memoire’, meaning ‘sites of memory’, as a place of “remembrance that exist(s) in a social world that constantly seeks to get ahead of itself, to “innovate” (Nafus and Anderson in Cefkin 2009, 141). The concept of ‘festival memory’ has not yet been explored in any depth, but such significant shifts in festivals such as BIFF are arguably sites where festival histories and identities, and film knowledge itself, can be irretrievably lost.

Evoking poetics of memory through performing site: Naik Naik, a Malaysian Australian collaboration in the world heritage setting of Melaka

Memory, time and metaphor are central triggers for artists in exploring and shaping their creative work. This paper examines the place of artists as ‘memory-keepers’, and ‘memory-makers’, in particular through engagement with the time-based art of site-specific performance. Naik Naik (Ascent) was a multi-site performance project in the historic setting of Melaka, Malaysia, and is partially recaptured through the presence and voices of its collaborating artists. Distilled from moments recalled, this paper seeks to uncover the poetics of memory to emerge from the project; one steeped in metaphor rather than narrative. It elicits some of the complex and interdependent layers of experience revealed by the artists in Naik Naik; cultural, ancestral, historical, personal, instinctual and embodied memories connected to sound, smell, touch, sensation and light, in a spatiotemporal context for which site is the catalyst. The liminal nature of memory at the heart of Naik Naik, provides a shared experience of past and present and future, performatively interwoven.

The role of moral disengagement in underage drinking and heavy episodic drinking

Objectives The current study had two aims. First, to develop a moral disengagement scale contextualized to underage drinking. Second, to investigate Bandura’s (1986) self-regulatory model within the context of underage drinking. Method Two different samples of students participated in the study. The first sample included 619 (362 females) adolescents (Mage = 15.3 years, SD = 1.09 years) and the second sample 636 (386 females) adolescents (Mage = 15.3 years, SD = 1.03 years). Students in the first sample completed the Underage Drinking Disengagement Scale (UDDS), and measures of engagement in underage drinking and heavy episodic drinking. Students in the second sample completed these measures as well as scales of general moral disengagement, personal standards and anticipatory guilt associated with underage drinking. Results For the UDDS, exploratory and confirmatory factor analyses verified a single factor structure. The UDDS was more strongly associated with engagement in underage drinking and heavy episodic drinking than a general measure of moral disengagement. A moderated mediation analysis revealed that adolescents who negatively evaluated underage drinking reported more anticipatory guilt, and more anticipatory guilt was associated with less engagement in underage drinking and less heavy episodic drinking. This relationship was weaker at high compared to low levels of underage drinking disengagement. Conclusions/Importance Understanding how adolescents self-regulate their drinking, and ways that such self-regulation may be deactivated or disengaged, may help identify those adolescents at increased risk of drinking underage and of engaging in heavy episodic drinking.

A combination of local inflammation and central memory T cells potentiates immunotherapy in the skin

Adoptive T cell therapy uses the specificity of the adaptive immune system to target cancer and virally infected cells. Yet the mechanism and means by which to enhance T cell function are incompletely described, especially in the skin. In this study, we use a murine model of immunotherapy to optimize cell-mediated immunity in the skin. We show that in vitro - derived central but not effector memory-like T cells bring about rapid regression of skin-expressing cognate Ag as a transgene in keratinocytes. Local inflammation induced by the TLR7 receptor agonist imiquimod subtly yet reproducibly decreases time to skin graft rejection elicited by central but not effector memory T cells in an immunodeficient mouse model. Local CCL4, a chemokine liberated by TLR7 agonism, similarly enhances central memory T cell function. In this model, IL-2 facilitates the development in vivo of effector function from central memory but not effector memory T cells. In a model of T cell tolerogenesis, we further show that adoptively transferred central but not effector memory T cells can give rise to successful cutaneous immunity, which is dependent on a local inflammatory cue in the target tissue at the time of adoptive T cell transfer. Thus, adoptive T cell therapy efficacy can be enhanced if CD8+ T cells with a central memory T cell phenotype are transferred, and IL-2 is present with contemporaneous local inflammation. Copyright © 2012 by The American Association of Immunologists, Inc.

Steady-state dendritic cells expressing cognate antigen terminate memory CD8+ T-cell responses

Antigen stimulation of naive T cells in conjunction with strong costimulatory signals elicits the generation of effector and memory populations. Such terminal differentiation transforms naive T cells capable of differentiating along several terminal pathways in response to pertinent environmental cues into cells that have lost developmental plasticity and exhibit heightened responsiveness. Because these cells exhibit little or no need for the strong costimulatory signals required for full activation of naive T cells, it is generally considered memory and effector T cells are released from the capacity to be inactivated. Here, we show that steadystate dendritic cells constitutively presenting an endogenously expressed antigen inactivate fully differentiated memory and effector CD8+ T cells in vivo through deletion and inactivation. These findings indicate that fully differentiated effector and memory T cells exhibit a previously unappreciated level of plasticity and provide insight into how memory and effector T-cell populations may be regulated. © 2008 by The American Society of Hematology.

Targeting antigen to diverse APCs inactivates memory CD8+ T cells without eliciting tissue-destructive effector function

Memory T cells develop early during the preclinical stages of autoimmune diseases and have traditionally been considered resistant to tolerance induction. As such, they may represent a potent barrier to the successful immunotherapy of established autoimmune diseases. It was recently shown that memory CD8+ T cell responses are terminated when Ag is genetically targeted to steady-state dendritic cells. However, under these conditions, inactivation of memory CD8+ T cells is slow, allowing transiently expanded memory CD8+ T cells to exert tissue-destructive effector function. In this study, we compared different Ag-targeting strategies and show, using an MHC class II promoter to drive Ag expression in a diverse range of APCs, that CD8+ memory T cells can be rapidly inactivated by MHC class II+ hematopoietic APCs through a mechanism that involves a rapid and sustained downregulation of TCR, in which the effector response of CD8+ memory cells is rapidly truncated and Ag-expressing target tissue destruction is prevented. Our data provide the first demonstration that genetically targeting Ag to a broad range of MHC class II+ APC types is a highly efficient way to terminate memory CD8+ T cell responses to prevent tissue-destructive effector function and potentially established autoimmune diseases. Copyright © 2010 by The American Association of Immunologists, Inc.

Next generation sequencing identifies novel CACNA1A gene mutations in Episodic Ataxia type 2

Episodic Ataxia type 2 (EA2) is a rare autosomal dominantly inherited neurological disorder characterized by recurrent disabling imbalance, vertigo and episodes of ataxia lasting minutes to hours. EA2 is caused most often by loss of function mutations of the calcium channel gene CACNA1A. In addition to EA2, mutations in CACNA1A are responsible for two other allelic disorders: familial hemiplegic migraine type1 (FHM1) and spinocerebellar ataxia type 6 (SCA6). Herein, we have utilised Next Generation Sequencing (NGS) to screen the coding sequence, exon-intron boundaries and UTRs of five genes where mutation is known to produce symptoms related to EA2, including CACNA1A. We performed this screening in a group of 31 unrelated patients with EA2 symptoms. Both novel and known mutations were detected through NGS technology, and confirmed through Sanger sequencing. Genetic testing showed in total 15 mutation bearing patients (48%), of which 9 were novel mutations (6 missense and 3 small frameshift deletion mutations) and six known mutations (4 missense and 2 nonsense).These results demonstrate the efficiency of our NGS-panel for detecting known and novel mutations for EA2 in the CACNA1A gene, also identifying a novel missense mutation in ATP1A2 which is not a normal target for EA2 screening.

Memory and Gender in Medieval Europe 900-1200

Review of Memory and Gender in Medieval Europe, 900-1200 by Elizabeth van Houts (Toronto UP, 1999).