Hence, although the cellular or molecular mechanisms are not yet fully understood, these findings. These findings might merit investigation of the combination of the two treatment options for patients with ulcerative colitis. In addition, the significant decrease in the number of CD4 + T cells before the clinical onset of flare, as well as the significant increase in the number of CD4 + CD25med effector T cells and the even more marked increase in CD4 + CD25high regulatory T cells during active disease when compared to the time point pre-flare, should be subjected to further investigation of the pathophysiological concepts in UC. Our study had several important limitations. First, it was designed primarily as an efficacy trial, and the presented findings are the results of an exploratory analysis. Second, flare was defined clinically by the use of a clinical index, which involved patients’ subjective interpretation of symptoms rather than objective signs of inflammation. However, in most instances flare was confirmed by endoscopy and by elevated levels of blood and fecal inflammation markers, thus providing a more objective definition of acute inflammation. Finally, because the herbal preparation shows a slight trend toward lower efficacy, one could argue that the specific pattern may Z-VAD-FMK reflect a flare rather than a primary mechanism. However, the differences in T-cell populations during flares indicate a primary failure of the applied therapy, which is true for both investigated treatments. In conclusion, in UC patients experiencing an acute flare, populations of T cells and especially CD4 + CD25high regulatory T cells demonstrate a distinctly different pattern in response to treatment with the herbal preparation of myrrh, chamomile extract, and coffee charcoal than they demonstrate in response to treatment with mesalazine. These findings suggest an active repopulation of regulatory T cells during active disease. However, further studies are needed to clarify the mode of action of herbal treatment. Hypercholesterolemia is a critical step in the initiation of atherosclerosis. Public concern is rising because cardiovascular diseases including atherosclerosis, coronary heart disease, cerebrovascular disease, and hypertensive heart disease, are known to be the leading causes of death in the world. Therefore, effective dietary and therapeutic approaches to hypercholesterolemia are currently of general interest. In addition, some reports have suggested that RJ feeding ameliolates hypercholesterolemia in an experimental animal model and in human subjects. However, the active component and molecular mechanism underlying the hypocholesterolemic action of RJ have not yet been understood. It has been reported that dietary protein affects serum cholesterol levels. Vegetable proteins reduce serum cholesterol levels compared with animal proteins. Previous studies have clearly demonstrated that the hypocholesterolemic action of dietary protein and peptides is closely related to the bile acid-binding capacity of dietary protein and bile acid metabolism. Bile acids play important roles not only in the absorption of dietary fat as a detergent, but also in the regulation of cholesterol homeostasis via cholesterol degradation.