Open space office: A review of the literature and Hong Kong case studies.

BACKGROUND: Open plan or open space office has become increasingly popular but those who promote the concept seldom refer to health studies or workers' perceptions of a change in office layout towards an open space arrangement. OBJECTIVE: To review the literature on open plan or open space office layouts in terms of facilities management (FM) with users' perceptions in mind and to obtain opinions of users of open space offices for a better appreciation of the FM issues. METHODS: A literature search of research papers from 2007 in journals using the keywords "open plan office" and "open space office" plus "health", first in the titles then in the text, was carried out. Thirty-two of those papers, accessible by the authors' institutions, were consulted together with 5 other works in the Harvard Business Review. The review consulted but excluded papers and reports published or sponsored by commercial firms that were in favour of open space layouts. Case studies were conducted by face to face meetings in confidence with workers in the middle managements of twelve Hong Kong organisations known as friends to two of the authors. Problems as seen by staff are reported and discussed. RESULTS: The literature review reveals that apart from writing that promotes the use of an open plan office layout, a host of scientific works point to the problems of perceived dissatisfaction with such a layout, the nature of the dissatisfaction tending to depend on the actual design. Most workers interviewed disliked the new style open plan layouts, which points to the necessity of consulting workers when such changes are contemplated, as well as monitoring the results of the change once it is in place whether against workers' wishes or with their support. There is a need for a number of facility arrangements in making a change to open plan that ensures that worker needs for proper lighting, privacy, and indoor health will be met. CONCLUSIONS: If the aim of a change to an open plan arrangement is to promote collegial communications in office, the study sheds light on the extent to which such arrangements may not in practice be suitable for achieving the aim. It follows that further, more specifically sociological studies of workers' job satisfaction and emotional health in open plan office settings would be worth doing.

Neurofascin as a novel target for autoantibody-mediated axonal injury.

Axonal injury is considered the major cause of disability in patients with multiple sclerosis (MS), but the underlying effector mechanisms are poorly understood. Starting with a proteomics-based approach, we identified neurofascin-specific autoantibodies in patients with MS. These autoantibodies recognize the native form of the extracellular domains of both neurofascin 186 (NF186), a neuronal protein concentrated in myelinated fibers at nodes of Ranvier, and NF155, the oligodendrocyte-specific isoform of neurofascin. Our in vitro studies with hippocampal slice cultures indicate that neurofascin antibodies inhibit axonal conduction in a complement-dependent manner. To evaluate whether circulating antineurofascin antibodies mediate a pathogenic effect in vivo, we cotransferred these antibodies with myelin oligodendrocyte glycoprotein-specific encephalitogenic T cells to mimic the inflammatory pathology of MS and breach the blood-brain barrier. In this animal model, antibodies to neurofascin selectively targeted nodes of Ranvier, resulting in deposition of complement, axonal injury, and disease exacerbation. Collectively, these results identify a novel mechanism of immune-mediated axonal injury that can contribute to axonal pathology in MS.

Substance P selectively decreases paired pulse depression in the rat hippocampal slice.

BACKGROUND: Although being widespread in the hippocampus, the role tachykinins play in synaptic transmission is unclear. The effect of substance P on field potentials evoked by stimulation of the Schaffer collateral-commissural fibres and recorded from the CA1 region of the rat hippocampal slice were studied. RESULTS: Perfusion of substance P (8 microM) had no effect on the fEPSP or population spike. Substance P did however cause a selective reduction in the paired pulse depression of population spikes evoked by paired stimulation at interpulse intervals of 20-80 msec. A comparison of the actions of other tachykinin receptor agonists gave an order of potency of substance P > [beta-Ala8]-neurokinin A (4-10) > senktide. The effect of substance P was reduced by the neurokinin-1 receptor antagonist SR140333, but not by the neurokinin-2 or neurokinin-3 receptor antagonists, MDL 29,913 or [Trp7, beta-Ala8]-neurokinin A (4-10). CONCLUSION: The order of potency of the agonists, and the effects of the antagonists, both indicate that the effect of substance P on paired pulse depression is mediated by neurokinin-1 receptors.

An endogenous capsaicin-like substance with high potency at recombinant and native vanilloid VR1 receptors.

The vanilloid receptor VR1 is a nonselective cation channel that is most abundant in peripheral sensory fibers but also is found in several brain nuclei. VR1 is gated by protons, heat, and the pungent ingredient of "hot" chili peppers, capsaicin. To date, no endogenous compound with potency at this receptor comparable to that of capsaicin has been identified. Here we examined the hypothesis, based on previous structure-activity relationship studies and the availability of biosynthetic precursors, that N-arachidonoyl-dopamine (NADA) is an endogenous "capsaicin-like" substance in mammalian nervous tissues. We found that NADA occurs in nervous tissues, with the highest concentrations being found in the striatum, hippocampus, and cerebellum and the lowest concentrations in the dorsal root ganglion. We also gained evidence for the existence of two possible routes for NADA biosynthesis and mechanisms for its inactivation in rat brain. NADA activates both human and rat VR1 overexpressed in human embryonic kidney (HEK)293 cells, with potency (EC(50) approximately 50 nM) and efficacy similar to those of capsaicin. Furthermore, NADA potently activates native vanilloid receptors in neurons from rat dorsal root ganglion and hippocampus, thereby inducing the release of substance P and calcitonin gene-related peptide (CGRP) from dorsal spinal cord slices and enhancing hippocampal paired-pulse depression, respectively. Intradermal NADA also induces VR1-mediated thermal hyperalgesia (EC(50) = 1.5 +/- 0.3 microg). Our data demonstrate the existence of a brain substance similar to capsaicin not only with respect to its chemical structure but also to its potency at VR1 receptors.

Effect of cannabinoids on synaptic transmission in the rat hippocampal slice is temperature-dependent.

We have previously reported that the synthetic cannabinoid R-(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxazin-yl]-(1-naphthalenyl)methanone mesylate (WIN55,212-2) causes a selective inhibition of paired pulse depression of population spikes recorded from the CA1 region of rat hippocampal slices maintained at 28-30 degrees C. We now show that this effect is highly temperature-dependent and that WIN55,212-2 actually increases paired pulse depression of population spikes recorded from slices maintained at 35 degrees C. This temperature dependence was found to correlate with the effects of the known gamma-amino butyric acid (GABA)-uptake inhibitors, nipecotic acid and guvacine, which were without effect at 28-30 degrees C, but increased paired pulse depression at 35 degrees C. The results show that the effects of cannabinoids on synaptic transmission in the hippocampal slice are highly temperature-dependent and it is suggested that this is due to the presence of increased GABA uptake at higher temperatures.