FIT

The FIT Game III: Reducing the Operating Expenses of a Game-Based Approach to Increasing Healthy Eating in Elementary Schools.[Pubmed:28375645]

Games Health J. 2017 Apr;6(2):111-118.

OBJECTIVE: Previously published versions of the healthy eating "FIT Game" were administered by teachers in all grades at elementary schools. The present study evaluated whether the game would retain its efficacy if teachers were relieved of this task; presenting instead all game materials on visual displays in the school cafeteria. MATERIALS AND METHODS: Participants were 572 children attending two Title 1 elementary schools (grades K-5). Following a no-intervention baseline period in which fruit and vegetable consumption were measured from food waste, the schools played the FIT Game. In the game, the children's vegetable consumption influenced events in a good versus evil narrative presented in comic book-formatted episodes in the school cafeteria. When daily vegetable-consumption goals were met, new FIT Game episodes were displayed. Game elements included a game narrative, competition, virtual currency, and limited player autonomy. The two intervention phases were separated by a second baseline phase (within-school reversal design). Simulation Modeling Analysis (a bootstrapping technique appropriate to within-group time-series designs) was used to evaluate whether vegetable consumption increased significantly above baseline levels in the FIT Game phases (P < 0.05). RESULTS: Vegetable consumption increased significantly from 21.3 g during the two baseline phases to 42.5 g during the FIT Game phases; a 99.9% increase. The Game did not significantly increase fruit consumption (which was not targeted for change), nor was there a decrease in fruit consumption. CONCLUSION: Labor-reductions in the FIT Game did not reduce its positive impact on healthy eating.

Mu-, delta- and kappa-opioid receptor-mediated inhibition of neurotransmitter release and adenylate cyclase activity in rat brain slices: studies with fentanyl isothiocyanate.[Pubmed:2906610]

Eur J Pharmacol. 1988 Sep 13;154(2):169-78.

We investigated the effects of [D-Ala2,D-Leu5]enkephalin (DADLE). [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAGO), [D-Pen2,D-Pen5]enkephalin (DPDPE) (0.01-1 microM) and bremazocine (0.001-0.3 microM) on the electrically evoked release of radiolabelled neurotransmitters and on the dopamine (DA)-stimulated cyclic AMP efflux from superfused rat brain slices. The differential inhibitory effects of these agonists on the evoked neurotransmitter release indicate that the opioid receptors mediating presynaptic inhibition of [3H]noradrenaline (NA, cortex), [14C]acetylcholine (ACh, striatum) and [3H]DA (striatum) release represent mu, delta and kappa receptors, respectively. In agreement with this classification, preincubation (60 min) of the slices with the delta-opioid receptor-selective irreversible ligand, fentanyl isothiocyanate (FIT, 0.01-1 microM), antagonized the inhibitory effects of DADLE and DPDPE on striatal [14C]ACh release only. On the other hand, the D-1 DA receptor-stimulated cyclic AMP efflux from striatal slices appeared to be inhibited by activation of mu as well as of delta receptors. In this case, the reversible mu antagonist, naloxone (0.1 microM), fully antagonized the inhibitory effect of the mu agonist, DAGO, without changing the effect of the delta agonist DPDPE but was ineffective as an antagonist in slices pretreated with FIT (1 microM). The inhibitory effect of DAGO on the electrically evoked [3H]NA release was antagonized by naloxone whether the receptors were irreversibly blocked by FIT or not. These data not only further support the existence of independent presynaptic mu-, delta- and kappa-opioid receptors in rat brain but also evidence strongly that mu and delta receptors mediating the inhibition of DA-sensitive adenylate cyclase could share a common binding site (for naloxone and FIT) and, therefore, may represent constituents of a functional opioid receptor complex.

Evidence that the delta-selective alkylating agent, fit, alters the mu-noncompetitive opiate delta binding site.[Pubmed:2991807]

Neuropeptides. 1985 Jun;6(3):227-37.

Considerable evidence supports the notion that the prototypic delta agonist [3H]D-ala2-D-leu5-enkephalin labels two binding sites on brain membranes in vitro. Recent studies have demonstrated that treatment of brain membranes with the delta-selective, site-directed, alkylating agent, FIT (Rice et al., Science 220, 314-316, 1983) results in a membrane preparation devoid of detectable higher affinity [3H]D-ala2-D-leu5-enkephalin binding sites, but contain residual lower affinity binding sites at which mu-ligands are apparent noncompetitive inhibitors (Rothman et al., Neuropeptides 4:210-215, 1984). In this paper we extend these data by showing that although FIT eliminates the higher affinity binding site, it also alters the properties of the residual lower affinity binding sites.

Irreversible ligands with high selectivity toward delta and mu opiate receptors.[Pubmed:6132444]

Science. 1983 Apr 15;220(4594):314-6.

Alkylating agents that display strong selectivity for opiate receptor types delta or mu were prepared by appropriate modification of the structures of the strong analgesics fentanyl, etonitazene, and endoethenotetrahydrooripavine. The availability of these substances should facilitate studies of the structural basis of receptor specificity and of the physiologic roles of these receptors.