Effect of tiger nut-derived products in gluten-free batter and bread.

Tiger nut is a tuber used to produce tiger nut milk that yields a high quantity of solid waste, which can be dried and used as fiber source. The objective of this paper was to evaluate the quality of gluten-free bread formulated with different tiger nut-derived products in order to substitute soya flour (which is an allergen ingredient) and, at the same time, increase the use of tiger nut-derived products. Four gluten-free formulations based on corn starch and containing tiger nut milk, tiger nut milk by-product, tiger nut flour, or soya flour (as reference formulation) were studied. Tiger nut milk increased G' of gluten-free batter and rendered breads with the softest crumb (502.46 g ± 102.05), the highest loaf-specific volume (3.35 cm(3)/g ± 0.25), and it was mostly preferred by consumers (61.02%). Breads elaborated with tiger nut flour had similar characteristics than soya flour breads (except in color and crumb structure). The addition of tiger nut milk by-product resulted in a hard (1047.64 g ± 145.74) and dark (L(*) = 70.02 ± 3.38) crumb bread, which was the least preferred by consumers. Results showed that tiger nut is a promising ingredient to formulate gluten-free baked products.

Discovery of a novel class of zwitterionic, potent, selective and orally active S1P1 direct agonists.

Amido-1,3,4-thiadiazoles have been identified as a novel structural class of potent and selective sphingosine-1-phosphate receptor subtype 1 agonists. Starting from a micromolar HTS hit with the help of an in-house homology model, robust structural-activity relationships were developed to yield compounds with good selectivity and excellent in vivo efficacy in rat models.

Indolin-2-one p38α inhibitors III: bioisosteric amide replacement.

Crystallographic structural information was used in the design and synthesis of a number of bioisosteric derivatives to replace the amide moiety in a lead series of p38α inhibitors which showed general hydrolytic instability in human liver preparations. Triazole derivative 13 was found to have moderate bioavailability in the rat and demonstrated potent in-vivo activity in an acute model of inflammation.

Influence of final baking technologies in partially baked frozen gluten-free bread quality.

The effect of final baking in convection oven (FBC), microwave oven (FBM), and microwave oven with susceptor packaging material (FBMS) on partially baked (PB) frozen gluten-free bread characteristics was investigated. Specific volume and crust color of loaves were measured at day 0. Bread moisture, water activity, and crumb and crust texture (at 15, 45, and 90 min after baking) were analyzed at day 0 and after 28 d of frozen storage (-18 °C). Volatile compounds from breads baked in convection oven or microwave oven with susceptor packaging material were also evaluated. Bread finally baked in convection oven or in microwave oven with susceptor packaging increased crust browning. Crumb and roll hardness increased with time after final baking (measured at 15, 45, 90 min) and after 28 d of frozen storage. Bread finally baked in microwave oven was the hardest, due to high water losses. At day 0, bread finally baked in convection oven had softer crumb than bread finally baked in microwave oven with susceptor packaging but, after 28 d of frozen storage, there were no differences between them. Moreover, FBC and FBMS rendered gluten-free breads that could not be distinguished in a triangular test and had the same volatile compounds profile. In conclusion, FBMS could be an alternative to FBC.

The sphingosine-1-phosphate receptor-1 antagonist, W146, causes early and short-lasting peripheral blood lymphopenia in mice.

Agonists of the sphingosine-1-phosphate (S1P) receptors, like fingolimod (FTY720), are a novel class of immunomodulators. Administration of these compounds prevents the egress of lymphocytes from primary and secondary lymphoid organs causing peripheral blood lymphopenia. Although it is well established that lymphopenia is mediated by S1P receptor type 1 (S1P1), the exact mechanism is still controversial. The most favored hypothesis states that S1P1 agonists cause internalization and loss of the cell surface receptor on lymphocytes, preventing them to respond to S1P. Hence, S1P1 agonists would behave in vivo as functional antagonists of the receptor. For this hypothesis to be valid, a true S1P1 antagonist should also induce lymphopenia. However, it has been reported that S1P1 antagonists fail to show this effect, arguing against the concept. Our study demonstrates that a S1P1 antagonist, W146, induces a significant but transient blood lymphopenia in mice and a parallel increase in CD4+ and CD8+ lymphocytes in lymph nodes. Treatment with W146 also causes the accumulation of mature T cells in the medulla of the thymus and moreover, it induces lung edema. We show that both the S1P1 antagonist and a S1P1 agonist cause lymphopenia in vivo in spite of their different effects on receptor expression in vitro. Although the antagonist purely blocks the receptor and the agonist causes its disappearance from the cell surface, the response to the endogenous ligand is prevented in both cases. Our results support the hypothesis that lymphopenia evoked by S1P1 agonists is due to functional antagonism of S1P1 in lymphocytes.