MASTER’S PROJECT: CHALLENGING STRUCTURAL RACISM IN PHILANTHROPY THROUGH CREATIVE EXPRESSION AND DEEP LISTENING

This capstone project is an account of a personal transformation journey that started in March of 2017. It follows my deep and personal exploration of challenging systemic racism as I spoke with many leaders in the philanthropic and artistic communities. In addition, I created artwork to help incorporate and synthesize my emotions around white supremacy and process what I was learning. The qualitative information that was gathered was abundant and the supporting art journaling technique was useful in the translation of that information

Escherichia coli biofilm formation, motion and protein patterns on hyaluronic acid and polydimethylsiloxane depend on surface stiffness

International audienceSurface stiffness of the microenvironment is a mechanical signal regulating biofilm growth without the risks associated with the use of bioactive agents. However, mechanisms determining the expansion or prevention of biofilm growth on soft and stiff substrates are largely unknown. To answer this question, we used PDMS (polydimethylsiloxane, 9-574kPa) and HA (hyaluronic acid gels, 44Pa-2kPa) differing in hydration. We showed that softest HA inhibits Escherichia coli biofilm growth while stiffest PDMS activates it. The bacterial mechanical environment significantly regulates MscS mechanosensitive channel, in higher abundance on the least colonized HA-44Pa, and Type-1 pili (Fim A) in higher abundance on the most colonized PDMS-9kPa. Type 1 pili regulated free motion (capacity of bacteria to move far from it initial position) necessary for biofilm growth independently of the substrate surface stiffness. In contrast, the total length travelled by bacteria (diffusion coefficient) varied positively with surface stiffness but not with biofilm growth. The softest, hydrated HA, the least colonized surface, revealed the least diffusive and the least free-moving bacteria. This finally shows that customizing surface elasticity and hydration together is an efficient means of affecting bacterial mobility and attachment to the surface, and thus designing biomedical surfaces to deter biofilm growth

Intestinal Epithelial Toll-like Receptor 4 Deficiency Modifies the Response to the Activity-Based Anorexia Model in a Sex-Dependent Manner: A Preliminary Study

International audienceThe role of microbiota in eating disorders has recently emerged. Previous data reported that lipopolysaccharides induce anorexia and a decrease of body weight through the activation of toll-like receptor 4 (TLR4). In the activity-based anorexia (ABA) mouse model, an increase of TLR4 expression in intestinal epithelial cells (IEC) has been described. We thus aimed to characterize the role of TLR4 in IEC in the ABA model in male and female mice. For this purpose, Vill-CreERT2-TLR4 LoxP, which are depleted for TLR4 in IEC in response to 4-OH tamoxifen, were submitted (ABA) or not (CT) to the ABA procedure that combined free access to a running wheel and progressive time-limited access to food. We thus compared CT and ABA TLR4IEC−/− mice to CT and ABA TLR4IEC+/+ mice. In response to the ABA model, TLR4IEC+/+ male and female mice exhibited a body weight loss associated to a decrease of lean mass. In TLR4IEC−/− male mice, body weight loss was delayed and less pronounced compared to TLR4IEC+/+ male mice. We did not observe a difference of body weight loss in female mice. The body composition remained unchanged between TLR4IEC−/− and TLR4IEC+/+ mice in both sexes. In both sexes, ABA TLR4IEC+/+ mice exhibited an increase of food-anticipatory activity, as well as an increase of immobility time during the open field test. However, female TLR4IEC−/− mice showed a decrease of the time spent at the centre and an increase of the time spent at the periphery of the open field area, whereas we did not observe differences in the male mice. In conclusion, the invalidation of TLR4 in IEC modified the response to the ABA model in a sex-dependent manner. Further studies should decipher the underlying mechanisms