Given the dose-dependent efficacy of S. boulardii and the efficiency of microencapsulation in protecting the yeast from degradation, alginate microspheres could be of great interest in therapeutic applications of the yeast.
Traumatic brain injury (TBI) is one of the most severe injuries encountered in intensive care units. TBI patients exhibit protein wasting and gastrointestinal dysfunction, which may be risk factors for a septic state. Specific nutritional support may be required for these patients, and we hypothesize that standard nutritional support does not allow restoration of the nutritional state of TBI patients. A well-validated rat model of TBI by fluid percussion was used. Rats were randomized into three groups: healthy rats receiving standard chow diet ad libitum (AL), rats sustaining TBI and receiving standard chow diet (TBI), and rats sustaining TBI and receiving a standard enteral diet (TBI-EN) for 4 days. TBI in rats was characterized by anorexia, body weight loss (AL: +15 +/- 5 g versus TBI: -11 +/- 4 g and TBI-EN: -8 +/- 4 g; p < 0.05), decrease in nitrogen balance (AL: 2.9 +/- 0.2 g versus TBI: 1.0 +/- 0.2 g and TBI-EN: 0.2 +/- 0.2 g, p < 0.05) associated with decrease in muscular protein content (extensor digitorum longus [EDL]: AL: 36 +/- 2 mg versus TBI: 26 +/- 3 mg and TBI-EN: 28 +/- 2 mg; p < 0.05), and intestinal atrophy (ileum: AL: 673 +/- 42 mg versus TBI: 442 +/- 23 mg and TBI-EN: 377 +/- 27 mg; p < 0.05). Interestingly, standard enteral nutrition was not effective in restoring any of these parameters. This work confirms that TBI is associated with profound nutritional alterations and has a major impact on nitrogen metabolism and on intestinal trophicity. It also demonstrates that using standard enteral nutrition cannot reverse this phenomenon. Thus, developing new nutritional strategies to cover TBI patients' specific nutritional requirements appears mandatory.
Hepatic fibrosis is a major consequence of chronic liver disease such as non-alcoholic steatohepatitis which is undergoing a dramatic evolution given the obesity progression worldwide, and has no treatment to date. Hepatic stellate cells (HSCs) play a key role in the fibrosis process, because in chronic liver damage, they transdifferentiate from a "quiescent" to an "activated" phenotype responsible for most the collagen deposition in liver tissue. Here, using a diet-induced liver fibrosis murine model (choline-deficient amino acid-defined, high fat diet), we characterized a specific population of HSCs organized as clusters presenting simultaneously hypertrophy of retinoid droplets, quiescent and activated HSC markers. We showed that hypertrophied HSCs co-localized with fibrosis areas in space and time. Importantly, we reported the existence of this phenotype and its association with collagen deposition in three other mouse fibrosis models, including CCl 4-induced fibrosis model. Moreover, we have also shown its relevance in human liver fibrosis associated with different etiologies (obesity, non-alcoholic steatohepatitis, viral hepatitis C and alcoholism). In particular, we have demonstrated a significant positive correlation between the stage of liver fibrosis and HSC hypertrophy in a cohort of obese patients with hepatic fibrosis. These results lead us to conclude that hypertrophied HSCs are closely associated with hepatic fibrosis in a metabolic disease context and may represent a new marker of metabolic liver disease progression.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.