The development of the divided profession in Queensland

The structure of the Queensland legal profession today is a product of a series of historical developments that can be traced to the beginnings of the legal profession in England. A proper understanding of the present practice and structure of the Australian legal profession needs an understanding of these English origins and then of the profession's introduction into Australia. It is proposed, therefore, to give a brief outline of the development of the legal profession in England and then to deal with the early years of the profession in the Colony of New South Wales after British settlement. The article will then describe the development of the profession in Queensland after separation from New South Wales in 1859 with some emphasis on the major changes relating to the roles of barristers and solicitors.

Selective down-regulation of the astrocyte glutamate transporters GLT-1 and GLAST within the medial thalamus in experimental wernicke's encephalopathy

Although earlier studies on thiamine deficiency have reported increases in extracellular glutamate concentration in the thalamus, a vulnerable region of the brain in this disorder, the mechanism by which this occurs has remained unresolved. Treatment with pyrithiamine, a central thiamine antagonist, resulted in a 71 and 55% decrease in protein levels of the astrocyte glutamate transporters GLT-1 and GLAST, respectively, by immunoblotting in the medial thalamus of day 14 symptomatic rats at loss of righting reflexes. These changes occurred prior to the onset of convulsions and pannecrosis. Loss of both GLT-1 and GLAST transporter sites was also confirmed in this region of the thalamus at the symptomatic stage using immunohistochemical methods. In contrast, no change in either transporter protein was detected in the non-vulnerable frontal parietal cortex. These effects are selective; protein levels of the astrocyte GABA transporter GAT-3 were unaffected in the medial thalamus. In addition, astrocyte-specific glial fibrillary acidic protein (GFAP) content was unchanged in this brain region, suggesting that astrocytes are spared in this disorder. Loss of GLT-1 or GLAST protein was not observed on day 12 of treatment, indicating that down-regulation of these transporters occurs within 48 h prior to loss of righting reflexes. Finally, GLT-1 content was positively correlated with levels of the neurofilament protein alpha -internexin, suggesting that early neuronal drop-out may contribute to the down-regulation of this glutamate transporter and subsequent pannecrosis. A selective, focal loss of GLT-1 and GLAST transporter proteins provides a rational explanation for the increase in interstitial glutamate levels, and may play a major role in the selective vulnerability of thalamic structures to thiamine deficiency-induced cell death.

Characterization of a glycine receptor domain that controls the binding and gating mechanisms of the beta-amino acid agonist, taurine

The beta -amino acid, taurine, is a full agonist of the human glycine receptor al subunit when recombinantly expressed in a mammalian (HEK293) cell line, but a partial agonist of the same receptor when expressed in Xenopus oocytes. Several residues in the Ala101-Thr112 domain have previously been identified as determinants of beta -amino acid binding and gating mechanisms in Xenopus oocyte-expressed receptors. The present study used the substituted cysteine accessibility method to investigate the role of this domain in controlling taurine-specific binding and gating mechanisms of glycine receptors recombinantly expressed in mammalian cells. Asn102 and Glu103 are identified as taurine and glycine binding sites, whereas Ala101 is eliminated as a possible binding site. The N102C mutation also abolished the antagonistic actions of taurine, indicating that this site does not discriminate between the putative agonist- and antagonist-bound conformations of beta -amino acids. The effects of mutations from Lys104-Thr112 indicate that the mechanism by which this domain controls beta -amino acid-specific binding and gating processes differs substantially depending on whether the receptor is expressed in mammalian cells or Xenopus oocytes. Thr112 is the only domain element in mammalian cell-expressed GlyRs which was demonstrated to discriminate between glycine and taurine.

Asymmetric contribution of α and β subunits to the activation of αβ heteromeric glycine receptors

This study investigated the role of beta subunits in the activation of alphabeta heteromeric glycine receptor (GlyR) chloride channels recombinantly expressed in HEK293 cells. The approach involved incorporating mutations into corresponding positions in alpha and beta subunits and comparing their effects on receptor function. Although cysteine-substitution mutations to residues in the N-terminal half of the alpha subunit M2-M3 loop dramatically impaired the gating efficacy, the same mutations exerted little effect when incorporated into corresponding positions of the beta subunit. Furthermore, although the alpha subunit M2-M3 loop cysteines were modified by a cysteine-specific reagent, the corresponding beta subunit cysteines showed no evidence of reactivity. These observations suggest structural or functional differences between alpha and beta subunit M2-M3 loops. In addition, a threonine-->leucine mutation at the 9' position in the beta subunit M2 pore-lining domain dramatically increased the glycine sensitivity. By analogy with the effects of the same mutation in other ligand-gated ion channels, it was concluded that the mutation affected the GlyR activation mechanism. This supports the idea that the GlyR beta subunit is involved in receptor gating. In conclusion, this study demonstrates that beta subunits contribute to the activation of the GlyR, but that their involvement in this process is significantly different to that of the alpha subunit.

Lawyers and the third dimension : A Solicitor v Council of the Law Society of New South Wales

Casenote and comment on the High Court case of A Solicitor v Council of the Law Society of New South Wales which dealt with the issue of whether a solicitor, convicted of aggravated indecent assault, should be allowed to continue practicing law.

Role of proline residues in the expression and function of the human noradrenaline transporter

The aim was to investigate the roles of proline residues in extracellular loop 2 (P172, P183, P188 and P209) and transmembrane domains 2, 5, 11 and 12 (P108, P270, P526, P551, P552 and P570) in determining noradrenaline transporter (NET) expression and function. Mutants of human NET with these residues mutated to alanine were pharmacologically characterized. Mutation of P108, P270 and P526 disrupted cell surface expression, from [H-3]nisoxetine binding and confocal microscopy data. Mutations of P526, P551 and P570 reduced transporter turnover (V-max of [H-3]noradrenaline uptake/B-max of [H-3]nisoxetine binding) by 1.5-1.7-fold compared with wild-type NET, so these residues might be involved in conformational changes associated with substrate translocation. Conversely, mutations of P172, P183, P188 and P209 increased V-max/B-max by 2-3-fold compared with wild-type, indicating that the presence of these proline residues limits turnover of the NET. The mutations had few effects on apparent affinities of substrates or affinities of inhibitors, except decreases in inhibitor affinities after mutations of the P270 and P570 residues, and increases after mutation of the P526 residue. Hence, proline residues in extracellular loop 2 and in transmembrane domains have a range of roles in determining expression and function of the NET.

Do chimpanzees (Pan troglodytes) and 2-year-old children (Homo sapiens) understand double invisible displacement?

Chimpanzees (Pan troglodytes) and young children (Homo sapiens) have difficulty with double invisible displacements in which an object is hidden in two nonadjacent boxes in a linear array. Experiment 1 eliminated the possibility that chimpanzees' previous poor performance was due to the hiding direction of the displacement device. As in Call (2001), subjects failed double nonadjacent displacements, showing a tendency to select adjacent boxes. In Experiments 2 and 3, chimpanzees and 24-month-old children were tested on a new adaptation of the task in which four hiding boxes were presented in a diamond-shaped array on a vertical plane. Both species performed above chance on double invisible displacements using this format, suggesting that previous poor performance was due to a response bias or inhibition problem rather than a fundamental limitation in representational capacity.

The development of self-recognition in mirrors and live videos

By 24-months of age most children show mirror self-recognition. When surreptitiously marked on their forehead and then presented with a mirror, they explore their own head for the unexpected mark. Here we demonstrate that self-recognition in mirrors does not generalize to other visual feedback. We tested 80 children on mirror and live video versions of the task. Whereas 90% of 24-month olds passed the mirror version, only 35% passed the video version. Seventy percent of 30-month olds showed video selfrecognition and only by age 36-months did the pass rate on the video version reach 90%. It remains to be y 24-months of age most children show mirror self-recognition. When surreptitiously marked on their forehead and then presented with a mirror, they explore their own head for the unexpected mark. Here we demonstrate that self-recognition in mirrors does not generalize to other visual feedback. We tested 80 children on mirror and live video versions of the task. Whereas 90% of 24-month olds passed the mirror version, only 35% passed the video version. Seventy percent of 30-month olds showed video selfrecognition and only by age 36-months did the pass rate on the video version reach 90%. It remains to be