A new method for the determination of lipolytic activity (LA) in milled products from cereals is described. This method is based on the use of the pHstat titration of free fatty acids (FFA) released by LA after incubating a mixture of defatted wholemeal or milling wheat fraction and olive oil during 72 hours at selected conditions of temperature and activity of water (A w ). The results given by this method have been compared systematically to those given by the time-consuming and classic one of the determination of the LA in low moisture media based upon the FFA determination by gas chromatography (GC) after separation by thin layer chromatography. The two methods have been used under various experimental conditions in order to study the effects of temperature, A w and addition of exogenous lipase in different wheat milled products. For the germ, bran, flour and whole meal fractions at 30°C and A w = 0.8, LA determined by the titration pHstat method was correlated to the values obtained by the GC method (r = 0.99). By pHstat, LA was found equal to 0.054, 0.75, 0.29 and 0.51 µmol.h -1 .g -1 (dm) vs 0.053, 0.79, 0.27 and 0.48 µmol.h -1 .g -1 (dm) by GC for the flour, bran, germ and wholemeal fraction respectively. When experimental conditions were modified, LA determined by pHstat was correlated with LA obtained by GC either when A w was varied for the bran fraction between 0.17 and 0.87 or temperature between 30 and 40°C (r = 0.95) or after addition of exogenous lipase to wheat flour (r = 0.97). This less time-consuming method for the determination of LA may be of a great interest to improve the storage conditions of cereal milled products as well as to estimate the efficiency of heat treatments on the denaturation of endogenous lipase in these products.

Studying the dynamic of gene regulatory networks is essential in order to understand the specific signals and factors that govern cell proliferation and differentiation during development. This also has direct implication in human health and cancer biology. The general transcriptional elongation regulator P-TEFb regulates the transcriptional status of many developmental genes. Its biological activity is controlled by an inhibitory complex composed of HEXIM and the 7SK snRNA. Here, we examine the function of HEXIM during Drosophila development. Our key finding is that HEXIM affects the Hedgehog signaling pathway. HEXIM knockdown flies display strong phenotypes and organ failures. In the wing imaginal disc, HEXIM knockdown initially induces ectopic expression of Hedgehog (Hh) and its transcriptional effector Cubitus interuptus (Ci). In turn, deregulated Hedgehog signaling provokes apoptosis, which is continuously compensated by apoptosis-induced cell proliferation. Thus, the HEXIM knockdown mutant phenotype does not result from the apoptotic ablation of imaginal disc; but rather from the failure of dividing cells to commit to a proper developmental program due to Hedgehog signaling defects. Furthermore, we show that ci is a genetic suppressor of hexim. Thus, HEXIM ensures the integrity of Hedgehog signaling in wing imaginal disc, by a yet unknown mechanism. To our knowledge, this is the first time that the physiological function of HEXIM has been addressed in such details in vivo.

Mantle Cell Lymphoma (MCL) is one of the worst lymphomas with a median overall survival of 3 to 4 years. Even if the use of rituximab was a great step in therapy, patients commonly develop resistance and relapse. New therapies or complement of existing therapies should be developed. Using spectrofluorimetry, we found that the resting cytosolic Ca 2+ ion concentration [Ca 2+ ] cyt of MCL patients cells and MCL cell lines was increased. This increase is correlated with a larger store-operated calcium entry (SOCE) amplitude which is responsible for the Ca 2+ ions influx. Furthermore, using a SOCE potentiating agent, we demonstrated that in the MCL Rec-1 cell line, the SOCE is already activated in resting conditions. Interestingly, this potentiating agent alone, by disturbing the SOCE, induced the apoptosis of Rec-1 cells with the same efficacy than rituximab. The use of the potentiating agent in addition to rituximab strengthens the rituximab-induced apoptosis of rituximab-sensitive Granta-519 and Rec-1 cells. However, this potentiating agent cannot convert the Jeko-1 rituximab-resistant to a rituximab-sensitive cell line. Our results confirm that the use of compound acting on the Ca 2+ homeostasis could be a new target of interest in complement to existing therapies.