These results demonstrate cortisol control of PPARγ expression in CEC, highlighting cortisol production deficiency in colonocytes as a key molecular event in the pathophysiology of UC.

Since the discovery in 1995 of α-galactosylceramide 1 (α-GalCer), also known as KRN7000,1 hundreds of compounds have been synthesized in order to activate invariant natural killer T (iNKT) cells. Such keen interest for this lymphocyte cell type is due to its ability to produce different cytokines that bias the immune response toward a Th1 or Th2 profile. Thus, an understanding of the immune polarization mechanism via iNKT activation may pave the way toward new therapeutics in various domains including cancer and infectious and autoimmune diseases. In this review, we propose an up-to-date analysis of iNKT activators associated with a structure-activity relationship (SAR) study aimed at complementing available reviews by highlighting molecular bases for a selective immune response.

Heart rate variability (HRV) depends on various reflexes, including the baroreflex or respiratory reflex. Experimental studies have suggested that the sinoatrial node density in G protein-linked receptors may be involved. Transgenic mice, with a specific eightfold atrial overexpression of human beta 1-adrenoceptor (beta 1-AR), have been generated to evaluate the role of the atrial beta 1-AR density on HRV. The heart rate was monitored using telemetry, and the signal was analyzed using a quantitative time-frequency domain analysis, the smoothed pseudo-Wigner-Ville method, and phase portrait maps. 1) Heart rate was unchanged, but the two normal components of HRV were decreased in transgenic mice. Transgenic mice have an unshortened life span and no arrhythmias. 2) Challenge of the animals by propranolol showed no modulation of the HRV in transgenic mice compared with controls. 3) In isolated atrial strips from transgenic mice, basal contractility was increased and there was no isoproterenol-induced inotropic effect. 4) The basal level of adenosine 3',5'-cyclic monophosphate production was lowered in transgenic mice, suggesting a shift in adenylate cyclase isoforms.