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Web tools are used to enrich the learning experience for students, and ease the administrative burden for lecturers a genuine win-win situation. This short paper highlights how at Portsmouth we use our HCI website to support the formative and summative assessment of a large group of final year undergraduates studying a 20 credit unit in HCI.

Mucosal mast cells (MMC) or their precursors migrate through the intestinal lamina propria to reside intraepithelially, where expression of mouse mast cell protease-1 indicates the mature phenotype. Alterations in expression of integrins that govern cell adhesion to the extracellular matrix may regulate this process. As the key cytokine mediating differentiation of mouse mast cell protease-1-expressing MMC homologues in vitro, TGF-β1 was considered a likely candidate for regulation of the integrins that facilitate intraepithelial migration of MMC. Therefore, we examined adhesion of bone marrow-derived mast cells cultured with and without TGF-β1 to laminin-1, fibronectin, and vitronectin along with expression of integrins likely to regulate this adhesion. Adhesion of PMA-stimulated cultured mast cells to laminin-1 increased from 5.3 ± 3.6% (mean ± SEM) in the absence of TGF-β1 to 58.7 ± 4.0% (p < 0.05) when cultured mast cells had differentiated into MMC homologues in the presence of TGF-β1. Increased adhesion of MMC homologues to laminin-1 was also stimulated by FcεRI cross-linking and the calcium ionophore A23187. Expression of the laminin-binding integrin α7 by MMC homologues grown in the presence of TGF-β1 was demonstrated by RT-PCR and flow cytometry, and preincubation of MMC homologues with the α7-neutralizing Ab 6A11 inhibited adhesion to laminin-1 by 98% (p < 0.05), demonstrating a novel role for this molecule in adhesion of a hemopoietic cell to laminin-1.

L-2-Chloropropionic acid (L-CPA), when orally administered at single high dose to rats produces a selective lesion in the cerebellum involving destruction of a high proportion of granule cells by a mechanism which involves N-methyl-D-aspartate (NMDA) receptors. Receptor binding studies demonstrated that L-CPA a had low affinity at the glutamate and glycine binding sites at NMDA receptors (530-660 microM), respectively, whereas L-CPA did not displace [3H]AMPA, [3H]NBQX or [3H]kainate from AMPA or kainate receptors. Whole cell-patch clamp experiments using cultured granule cells failed to demonstrate changes in membrane potential of cultured granule cells when either L-CPA (0.25 or 1 microM) was added alone to the bathing solution, or in combination with glycine (10 microM). Furthermore L-CPA did not alter the magnitude of the inward current produced by application of NMDA (100 microM)) to cultured granule cells, in the presence of glycine, as measured by patch clamp techniques. Experiments were also performed to discover whether L-CPA may alter the release of the excitatory amino acids from the cerebellum, which may then indirectly alter activity at glutamate receptors, leading to neuronal cell death. L-CPA (2 mM) did not affect either basal or stimulated (electrical or high potassium) endogenous aspartate release from superfused cerebellar slices nor did it alter the basal or stimulated release of [3H]aspartate from preloaded slices when introduced into the superfusion medium over 30 min. However, when cerebellar slices were preincubated with 2 mM L-CPA for 2 h at concentrations that are known to be neurotoxic to the brain in vivo, but not in vitro, the stimulated endogenous glutamate and aspartate net release was significantly attenuated, as compared to controls. Basal release was not significantly affected by the introduction of L-CPA-induced cerebellar neurotoxicity may be related to the inhibition of excitatory amino acid release from the cerebellum. In conclusion, although L-CPA does not appear to directly alter NMDA receptor activity the L-CPA-induced cerebellar neurotoxicity may be related to the inhibition of excitatory amino acid release from the cerebellum.

There is a growing realization that it may be expeditious to combine elements from different theories of learning when trying to derive a coherent and usable policy towards computer‐mediated learning. Consideration of the subtle distinction between Computer‐Aided Learning (CAL) and Computer‐Aided Instruction (CAI) conform the basis of a possible classification of computer‐mediated learning, and hence of multimedia tools. This classification enables the development of a continuum upon which to place various strategies for computer‐mediated learning, and hence a means of broadly classifying multimedia learning tools.