This indicates that the proportions of IL-18R-expressing hepatic c4 and c13 cells may be higher at the beginning of their generation than at later periods, and hence, the impact of IL-18 upon MCPHT cells may be the largest at the beginning of their generation and be attenuated as those T cells acquire the capacity to produce IL-4 and expand. Moreover, when IL-4-producing Th2 cells are induced, the downregulation of IL-18R expression upon those cells might be accelerated. Indeed, both the proportions and absolute numbers of MCPHT cells peaked at 6–7 weeks PI, and they gradually decreased after that period despite the existence of IL-18 in the environment. This may also suggest that MCPHT cells induced during the transition phase might act as one of the cellular sources of initial IL-4, which triggers Th2 cell generation, and as a ‘bridge’ connecting early Th1 and later Th2 phases of S. mansoni infection, which helps the appropriate phase transition within the liver. Further study will provide us with new tools to prevent and/or to treat hepatic granulomatous disorder induced following S. mansoni infection. Left ventricular hypertrophy, which develops due to pressure overload in patients with aortic stenosis, is associated with increased mortality and morbidity before and after aortic valve surgery. The lack of an evident correlation between the stenosis-dependent pressure load and the degree of LVH suggests that the left ventricular phenotype is dependent on a polygenic background. The familial predisposition of LVH is supported by several studies. Angiotensin II is known to promote hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Angiotensin II is generated locally in the cardiac tissue independently of circulating angiotensin II, and chymase has been found to be the major angiotensin II–producing enzyme in the human heart. In response to pathological conditions, such as pressure or volume overload, myocardial infarction, and diabetes, the locally generated angiotensin II contributes to the development of cardiac hypertrophy and fibrosis. Chymase is also involved in the activation of TGF-b in endothelial cells and in the heart. It has been shown that TGF-b plays an important role in the pathogenesis of fibrotic and hypertrophic remodeling in the pressure-overloaded heart, both in animal models and in patients with aortic stenosis. The expression of the chymase gene and its enzymatic activity in cardiac tissue was found to gradually increase over time in a hamster model of pressure overload hypertrophy, and several studies have suggested the role of chymase in left ventricular remodeling. The CMA1 gene is located on the long arm of chromosome 14, and its polymorphisms are associated with asthma nm repeat), atopic eczema, heart failure of nonischemic etiology, and low ejection fraction. However, no functional polymorphism has yet been reported.