More significant associations with BMD levels; therefore, a larger and perhaps more inclusive study, such as a study of postmenopausal women of multiple races, may be beneficial in this regard. None of the gene polymorphisms that were studied in this paper, even those of CALM3, were found to be associated with any other body composition levels. It is possible that the effects of other potential unidentified factors, such as socioeconomic status and diet, may mask the effects of the variances in these target genes on body composition given that age and smoking were the only two covariates that were adjusted for. This study, although limited in scope due to its focus on postmenopausal Caucasian woman, provides multiple opportunities for further investigation. A study of the impact of CALM3 and other target genes on BMD across several race/ethnicity groups may be informative because racial differences in BMD have been well established in the literature. This study demonstrates that genetic polymorphisms in genes that are involved in bone metabolism may impact BMD at least in Caucasian women. Further research is required to elucidate whether these polymorphisms and others that are yet to be discovered may also partially underlie the racial differences that are observed in BMD. Hepatitis C virus infection affects about 170 million U0126 people worldwide; the acute phase of infection is rarely cleared and most of patients become chronically infected. Chronic infection by HCV is often characterized by lipid metabolism disorders that lead to hepatic steatosis. In addition, lipid metabolism and cholesterol have a key role in viral life cycle. In particular, plasma membrane cholesterol is required for HCV entry ; moreover, HCV replication takes place in cholesterol rich domains within the viral replication complex. Recently, higher dietary cholesterol intake was associated with the progression of HCV related liver disease progression. Therefore, dietary modulation of cholesterol intake may represent an innovative strategy to reduce the progression of HCV infection. HCV usually induces robust immune responses, however it frequently escapes the immune defense to establish persistent infection. Although the underlying mechanisms for HCV persistence and disease pathogenesis are not fully understood, a role for interleukin -17-producing CD4+ T cells, also named Thelper 17 cells, has been proposed. Th17 cells produce IL-17A together with other cytokines, such as IL-17F, IL-21, and IL-22, and express CD161, that gives to these cells a specific liver homing phenotype. In particular, Th17 cells have been described as the principal mediators not only in autoimmune diseases but especially in chronic inflammatory disorders. Several authors described an increased amount of circulating and intrahepatic Th17 cells in Chronic Hepatitis C patients which correlates with the severity of liver inflammation. Notably, the development of Th17 cells is reciprocally interconnected with that of regulatory T cells.