Human inquiry: Steps towards emancipatory practice

In this paper we explore the contribution of work in Human Inquiry to the debate about what might constitute authentic emancipatory practice and about how such an ideal might be approached. We beghin by considering some key values, issues, and commitments which characterise this work and distinguish it from other established research traditions. A number of distinct approaches to the practice of human inquiry have been articulated. These are referred to but it is not our purpose to review particular approaches in detail here. Rather our aim is to move from this overview of human inquiry to consider some important implications for practice. In particular, we look at Bateson's theory of levels of learning and explore ways in which both the intellectual and the more personal frameworks of participants can contribute to, and at times impede, the kinds of mutual learning with which human inquiries are concerned. We illustrate this discussion by drawing on examples from our own work in human inquiry. Here we aim to highlight particular implications and issues that might arise within human inquiries. One source of illustrations is Peter's work with general and complementary practitioners in a primary health care centre, the other is Anne's work with UWE student groups acting as consultants for local community organisations. In each case we consider some origins, forms, and expressions of power differences and show how empowerment can occur as participants learn within and across Bateson's levels as inquiries progress. We conclude by summarising the evidence of and opportunities for empowerment in each case and by showing how a deeper appreciation of Bateson's levels of learning can further understanding of the nature of emancipatory practice. Finally, we make more general suggestions about the role of approaches to Human Inquiry in future emancipatory practice.     

Parameters for reliable results in genetic association studies in common disease.

It is increasingly apparent that the identification of true genetic associations in common multifactorial disease will require studies comprising thousands rather than the hundreds of individuals employed to date. Using 2,873 families, we were unable to confirm a recently published association of the interleukin 12B gene in 422 type I diabetic families. These results emphasize the need for large datasets, small P values and independent replication if results are to be reliable.     

Altered K+ movement in liver mitochondria from alloxan diabetic rats

Potassium movements were monitored in liver mitochondria from control and alloxan diabetic rats with a cationic electrode. There was net accumulation of K+ after Ca2+ addition to the mitochondria with the diabetic but not with the control.     

Explaining the excess of rare species in natural species abundance distributions

The observation that a few species in ecological communities are exceptionally abundant, whereas most are rare, prompted the development of species abundance models. Nevertheless, despite the large literature on the commonness and rarity of species inspired by these pioneering studies, some widespread empirical patterns of species abundance resist easy explanation. Notable among these is the observation that in large assemblages there are more rare species than the log normal model predicts. Here we use a long-term (21-year) data set, from an estuarine fish community, to show how an ecological community can be separated into two components. Core species, which are persistent, abundant and biologically associated with estuarine habitats, are log normally distributed. Occasional species occur infrequently in the record, are typically low in abundance and have different habitat requirements; they follow a log series distribution. These distributions are overlaid, producing the negative skew that characterizes real data sets.     

Low-temperature processing of 'baroplastics' by pressure-induced flow

The manufacturing of plastics traditionally involves melt processing at temperatures typically greater than 200 degrees C-to enable extrusion or moulding under pressure into desired forms-followed by solidification. This process consumes energy and can cause substantial degradation of polymers and additives (such as flame retardants and ultraviolet stabilizers), limiting plastics performance and recyclability. It was recently reported that the application of pressure could induce melt-like behaviour in the block copolymer polystyrene-block-poly(n-butyl methacrylate) (PS-b-PBMA), and this behaviour has now been demonstrated in a range of other block copolymer systems. These polymers have been termed baroplastics. However, in each case, the order-to-disorder transition, which gives rise to the accompanying change in rheology from soft solid to melt, was observed at temperatures far exceeding the glass transition temperatures (T(g)) of both components. Here we show that baroplastic systems containing nanophase domains of one high-T(g) and one low-T(g) component can exhibit melt-like flow under pressure at ambient temperature through an apparent semi-solid partial mixing mechanism that substantially preserves the high-T(g) phase. These systems were shredded and remoulded ten times with no evident property degradation. Baroplastics with low-temperature formability promise lower energy consumption in manufacture and processing, reduced use of additives, faster production and improved recyclability, and also provide potential alternatives to current thermoplastic elastomers, rubber-modified plastics, and semi-crystalline polymers.     

A structural state of the myosin V motor without bound nucleotide

The myosin superfamily of molecular motors use ATP hydrolysis and actin-activated product release to produce directed movement and force. Although this is generally thought to involve movement of a mechanical lever arm attached to a motor core, the structural details of the rearrangement in myosin that drive the lever arm motion on actin attachment are unknown. Motivated by kinetic evidence that the processive unconventional myosin, myosin V, populates a unique state in the absence of nucleotide and actin, we obtained a 2.0 A structure of a myosin V fragment. Here we reveal a conformation of myosin without bound nucleotide. The nucleotide-binding site has adopted new conformations of the nucleotide-binding elements that reduce the affinity for the nucleotide. The major cleft in the molecule has closed, and the lever arm has assumed a position consistent with that in an actomyosin rigor complex. These changes have been accomplished by relative movements of the subdomains of the molecule, and reveal elements of the structural communication between the actin-binding interface and nucleotide-binding site of myosin that underlie the mechanism of chemo-mechanical transduction.     

Xenoturbella is a deuterostome that eats molluscs

Xenoturbella bocki, first described in 1949 (ref. 1), is a delicate, ciliated, marine worm with a simple body plan: it lacks a through gut, organized gonads, excretory structures and coelomic cavities. Its nervous system is a diffuse nerve net with no brain. Xenoturbella's affinities have long been obscure and it was initially linked to turbellarian flatworms. Subsequent authors considered it variously as related to hemichordates and echinoderms owing to similarities of nerve net and epidermal ultrastructure, to acoelomorph flatworms based on body plan and ciliary ultrastructure (also shared by hemichordates), or as among the most primitive of Bilateria. In 1997 two papers seemed to solve this uncertainty: molecular phylogenetic analyses placed Xenoturbella within the bivalve molluscs, and eggs and larvae resembling those of bivalves were found within specimens of Xenoturbella. This molluscan origin implies that all bivalve characters are lost during a radical metamorphosis into the adult Xenoturbella. Here, using data from three genes, we show that the samples in these studies were contaminated by bivalve embryos eaten by Xenoturbella and that Xenoturbella is in fact a deuterostome related to hemichordates and echinoderms.     

Identification of the gene (BBS1) most commonly involved in Bardet-Biedl syndrome,a complex human obesity syndrome

Bardet-Biedl syndrome (BBS, OMIM 209900) is a genetic disorder with the primary features of obesity, pigmentary retinopathy, polydactyly, renal malformations, mental retardation and hypogenitalism. Individuals with BBS are also at increased risk for diabetes mellitus, hypertension and congenital heart disease. What was once thought to be a homogeneous autosomal recessive disorder is now known to map to at least six loci: 11q13 (BBS1), 16q21 (BBS2), 3p13 p12 (BBS3), 15q22.3 q23 (BBS4), 2q31 (BBS5) and 20p12 (BBS6). There has been considerable interest in identifying the genes that underlie BBS, because some components of the phenotype are common. Cases of BBS mapping ro BBS6 are caused by mutations in MKKS; mutations in this gene also cause McKusick-Kaufman syndrome (hydrometrocolpos, post-axial polydactyly and congenital heart defects). In addition, we recently used positional cloning to identify the genes underlying BBS2 (ref. 16) and BBS4 (ref. 17). The BBS6 protein has similarity to a Thermoplasma acidophilum chaperonin, whereas BBS2 and BBS4 have no significant similarity to chaperonins. It has recently been suggested that three mutated alleles (two at one locus, and a third at a second locus) may be required for manifestation of BBS (triallelic inheritance). Here we report the identification of the gene BBS1 and show that a missense mutation of this gene is a frequent cause of BBS. In addition, we provide data showing that this common mutation is not involved in triallelic inheritance.