Suffix Coherence and Stress in Australian Languages

This paper offers a formal account of the diverse patterns of suffix coherence (the degree to which suffixes combine with other morphemes to form metrical feet) with respect to stress among Australian languages. In section 2, data is presented from five Australian languages which stress monomorphemic words in a similar fashion, but which differ with respect to suffix coherence. It is proposed that two distinct kinds of morphological boundary must be recognised: the boundary between a root and a suffix, and the boundary between two suffixes. In section 3 an analysis is proposed in terms of Optimality Theory (OT, Prince and Smolensky 1993 and much work following on from this), and it is argued in concluding that this approach is essentially the one required to account for the data. These languages have all received some previous attention from phonologists, and previous attempts to account for their stress patterns with respect to suffix coherence are discussed briefly in section 4. It is argued that none of these accounts is entirely plausible. Most fail because they do not acknowledge the distinction between the two kinds of boundary proposed in section 2. Some fail because the specific approach taken has created a theoryinternal paradox

Optional disagreement and the case for feature hierarchies

Jingulu (western Barkly Tablelands, Northern Territory, Australia (non-Pama-Nyungan)), the traditional language of the Jingili people, shows evidence for a hierarchical relationship between all four of its gender categories. Modifiers have separate forms for each of the four genders and usually appear in the same gender form as the head they modify. When disagreement occurs, masculine modifiers can found with heads of all four genders, while vegetable gender heads can be modified by neuter modifiers as well. While agreement is the norm, disagreement is always an available option, and appears never to be either mandated or ruled out in specific grammatical or semantic contexts

Losing Sight of Land: Tales of Dyslexia and Dyspraxia in Psychophysical Actor Training

This article reports on the findings of a research project into the impact of psychophysical actor training methods on neurodiverse students. It illustrates how the application of a Social Theory of Learning Difference reveals the mechanisms whereby these training methods dysconsciously discriminate against those students who are dyslexic and/or dyspraxic learners. The research findings recognise the inherent value of psychophysical methods in the training of actors but suggests that there is a need to move away from a singular Psycho-Medical Theory of Learning Difference and to adopt a framework of learning difference based on the Social Model of (dis)ability, which requires institutions to adapt their provision to better meet a diverse range of needs. A revision of psychophysical approaches is proposed, which draws on a neuroscientific theory of experiential practice and a psychological framework of actor engagement. This new approach seeks to enhance the effective communication of embodied knowledge and skills in diverse actor training contexts and to allow students who are dyslexic and/or dyspraxic learners equal access to that learning

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Vaccination with a non-human random sequence amyloid oligomer mimic results in improved cognitive function and reduced plaque deposition and micro hemorrhage in Tg2576 mice

BACKGROUND: It is well established that vaccination of humans and transgenic animals against fibrillar Aβ prevents amyloid accumulation in plaques and preserves cognitive function in transgenic mouse models. However, autoimmune side effects have halted the development of vaccines based on full length human Aβ. Further development of an effective vaccine depends on overcoming these side effects while maintaining an effective immune response. RESULTS: We have previously reported that the immune response to amyloid oligomers is largely directed against generic epitopes that are common to amyloid oligomers of many different proteins and independent of a specific amino acid sequence. Here we have examined whether we can exploit this generic immune response to develop a vaccine that targets amyloid oligomers using a non-human random sequence amyloid oligomer. In order to study the effect of vaccination against generic oligomer epitopes, a random sequence oligomer (3A) was selected as it forms oligomers that react with the oligomer specific A11 antibody. Oligomer mimics from 3A peptide, Aβ, islet amyloid polypeptide (IAPP), and Aβ fibrils were used to vaccinate Tg2576 mice, which develop a progressive accumulation of plaques and cognitive impairment. Vaccination with the 3A random sequence antigen was just as effective as vaccination with the other antigens in improving cognitive function and reducing total plaque load (Aβ burden) in the Tg2576 mouse brains, but was associated with a much lower incidence of micro hemorrhage than Aβ antigens. CONCLUSION: These results shows that the amyloid Aβ sequence is not necessary to produce a protective immune response that specifically targets generic amyloid oligomers. Using a non-human, random sequence antigen may facilitate the development of a vaccine that avoids autoimmune side effects