Clinical efficacy of Lactobacillus reuteri-containing lozenges in the supportive therapy of generalized periodontitis stage III and IV,grade C: 1-year results of a double-blind randomized placebo-controlled pilot study

Clinical Oral Investigations - The aim of this 12-month mono-centre double-blind randomized placebo-controlled clinical study was to evaluate the efficacy of Lactobacillus reuteri-containing...     

Casein micelles from bovine Milk exerts Neuroprotection by stalling metabolic complications linked to oxidative brain injury

Metabolic Brain Disease - Caseins are the most abundant milk proteins in mammalian species and are assembled in supra-macromolecular structures called micelles. In this study, the microstructural...     

Weight loss reduces head motion: Revisiting a major confound in neuroimaging

Head motion during magnetic resonance imaging (MRI) induces image artifacts that affect virtually every brain measure. In parallel, cross‐sectional observations indicate a correlation of head motion with age, psychiatric disease status and obesity, raising the possibility of a systematic artifact‐induced bias in neuroimaging outcomes in these conditions, due to the differences in head motion. Yet, a causal link between obesity and head motion has not been tested in an experimental design. Here, we show that a change in body mass index (BMI) (i.e., weight loss after bariatric surgery) systematically decreases head motion during MRI. In this setting, reduced imaging artifacts due to lower head motion might result in biased estimates of neural differences induced by changes in BMI. Overall, our finding urges the need to rigorously control for head motion during MRI to enable valid results of neuroimaging outcomes in populations that differ in head motion due to obesity or other conditions.     

A thermogenic fat-epithelium cell axis regulates intestinal disease tolerance

Disease tolerance, the capacity of tissues to withstand damage caused by a stimulus without a decline in host fitness, varies across tissues, environmental conditions, and physiologic states. While disease tolerance is a known strategy of host defense, its role in noninfectious diseases has been understudied. Here, we provide evidence that a thermogenic fat–epithelial cell axis regulates intestinal disease tolerance during experimental colitis. We find that intestinal disease tolerance is a metabolically expensive trait, whose expression is restricted to thermoneutral mice and is not transferable by the microbiota. Instead, disease tolerance is dependent on the adrenergic state of thermogenic adipocytes, which indirectly regulate tolerogenic responses in intestinal epithelial cells. Our work has identified an unexpected mechanism that controls intestinal disease tolerance with implications for colitogenic diseases.

Resistance and disease tolerance are two distinct strategies a host can use to mitigate the negative impact of disease on tissue function and host fitness (1, 2). For example, during pathogenic infections, the detection and elimination of pathogens is mediated by resistance, whereas disease tolerance minimizes the negative impact of pathogens on host fitness without affecting pathogen burden. Although disease tolerance is a well-appreciated strategy of host defense against pathogens in both the plant and animal kingdoms (3–5), its importance in noninfectious diseases is largely unknown (1, 6).Recent studies have demonstrated that metabolic adaptations mediate disease tolerance during viral, bacterial, and parasitic infections (7–12). These findings suggest that disease tolerance programs are metabolically expensive and compete for energy with other tissue maintenance programs. Because homeothermy, the stable maintenance of core temperature, is a major energy consuming program in mammals (13), we postulated that it might energetically compete with disease tolerance programs to limit their expression in noninfectious diseases. We tested this hypothesis using murine models of colitis because the high regenerative capacity of the intestinal epithelium has been postulated to increase its intrinsic tolerance capacity (1).