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Articles by A. J Smith
Total Records ( 3 ) for A. J Smith
  A. J Smith and S. E. Tett

Objective. To design, implement and evaluate a novel intervention, utilizing electronic media, to improve benzodiazepine use in specific geographical areas in Australia.

Methods. An educational intervention about benzodiazepine use, using email, a website and bookmarks, targeted consumers, GPs, nurses (in aged care facilities) and pharmacists in two areas in Australia over a 6-month period. Two control areas, which received no aspect of the intervention, were used to compare and contrast. A drug use evaluation was conducted in aged care facilities before and after the study (in the intervention areas) and after the intervention (in the control areas) to assess quality of benzodiazepine use. Benzodiazepine dispensing data were obtained for each area before, during and after the intervention to quantitate use. Interviews were conducted with nurses and pharmacists involved in the intervention and website statistics were recorded.

Results. A significantly smaller number of aged care residents were on benzodiazepines for 6 months or more (P < 0.05) after the intervention compared with before. However, other indices, such as number of residents taking benzodiazepines or taking them for a long time, did not change significantly before compared to after the intervention and there were no significant differences between the control and intervention areas after the intervention. Quantitative use of benzodiazepines did not change after the intervention. Many health care professionals in the intervention areas remembered seeing the electronic educational material for benzodiazepines. The website was viewed 115 times during the study.

Conclusions. The study was easy and inexpensive to administer and attracted high participation rates by health care professionals. There was a change in the use of benzodiazepines in aged care facilities (less long-term benzodiazepine use) in the intervention areas. The electronic educational materials (emails and website) were read and informations (especially the key messages) were able to be recalled after the intervention. However, no large changes in benzodiazepine overall use (either between control and intervention areas or before and after the intervention) were recorded.

  M. H Tan , A. J Smith , B Pawlyk , X Xu , X Liu , J. B Bainbridge , M Basche , J McIntosh , H. V Tran , A Nathwani , T Li and R. R. Ali

Defects in the photoreceptor-specific gene encoding aryl hydrocarbon receptor-interacting protein-like 1 (AIPL1) are clinically heterogeneous and present as Leber Congenital Amaurosis, the severest form of early-onset retinal dystrophy and milder forms of retinal dystrophies such as juvenile retinitis pigmentosa and dominant cone-rod dystrophy. [Perrault, I., Rozet, J.M., Gerber, S., Ghazi, I., Leowski, C., Ducroq, D., Souied, E., Dufier, J.L., Munnich, A. and Kaplan, J. (1999) Leber congenital amaurosis. Mol. Genet. Metab., 68, 200–208.] Although not yet fully elucidated, AIPL1 is likely to function as a specialized chaperone for rod phosphodiesterase (PDE). We evaluate whether AAV-mediated gene replacement therapy is able to improve photoreceptor function and survival in retinal degeneration associated with AIPL1 defects. We used two mouse models of AIPL1 deficiency simulating three different rates of photoreceptor degeneration. The Aipl1 hypomorphic (h/h) mouse has reduced Aipl1 levels and a relatively slow degeneration. Under light acceleration, the rate of degeneration in the Aipl1 h/h mouse is increased by 2–3-fold. The Aipl1–/– mouse has no functional Aipl1 and has a very rapid retinal degeneration. To treat the different rates of degeneration, two pseudotypes of recombinant adeno-associated virus (AAV) exhibiting different transduction kinetics are used for gene transfer. We demonstrate restoration of cellular function and preservation of photoreceptor cells and retinal function in Aipl1 h/h mice following gene replacement therapy using an AAV2/2 vector and in the light accelerated Aipl1 h/h model and Aipl1–/– mice using an AAV2/8 vector. We have thus established the potential of gene replacement therapy in varying rates of degeneration that reflect the clinical spectrum of disease. This is the first gene replacement study to report long-term rescue of a photoreceptor-specific defect and to demonstrate effective rescue of a rapid photoreceptor degeneration.

  Y Yang , J Weiner , Y Liu , A. J Smith , D. J Huss , R Winger , H Peng , P. D Cravens , M. K Racke and A. E. Lovett Racke

The extent to which myelin-specific Th1 and Th17 cells contribute to the pathogenesis of experimental autoimmune encephalomyelitis (EAE) is controversial. Combinations of interleukin (IL)-1β, IL-6, and IL-23 with transforming growth factor β were used to differentiate myelin-specific T cell receptor transgenic T cells into Th17 cells, none of which could induce EAE, whereas Th1 cells consistently transferred disease. However, IL-6 was found to promote the differentiation of encephalitogenic Th17 cells. Further analysis of myelin-specific T cells that were encephalitogenic in spontaneous EAE and actively induced EAE demonstrated that T-bet expression was critical for pathogenicity, regardless of cytokine expression by the encephalitogenic T cells. These data suggest that encephalitogenicity of myelin-specific T cells appears to be mediated by a pathway dependent on T-bet and not necessarily pathway-specific end products, such as interferon and IL-17.

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