Again, APS significantly increased LDLR protein on hepatic cell surface. The specific mechanism for this regulation is unknown, but it could be possible that, similar to simvastatin, APS works through a negative feedback mechanism by depleting intracellular cholesterol pools. Our results revealed the decrease of plasma LDL-C was in agreement with the up-regulation of LDLR, which suggests APS may regulate cholesterol homeostasis partially through inducing LDL-R expression. It is of note that a significant reduction of HDL-C was seen in the current study after APS or simvastatin treatment. Other studies point out HDL is in high proportion of plasma cholesterol in hamsters. Consequently, a reduction of TC is usually accompanied by a decrease of HDL-C. On the other hand, HDL-C of hamsters contains high concentration of apo E and may thus be cleared by LDL-R. However, this SCH727965 CDK inhibitor effect is generally not translated to humans. In conclusion, these findings strongly suggest APS is a promising novel natural health hypolipidemic drug that may act by multiple mechanisms. APS lowers plasma cholesterol through a combination of inhibiting fractional cholesterol absorption, increasing fecal bile acid excretion, up-regulating hepatic LDL-R, cyp7a-1 gene expression. This study indicates that if proven in human trials, APS would provide an alternative to statins for patients with hyperlipidemia, atherosclerosis or coronary heart disease. Cellular clocks control important functions of the cell, such as circadian rhythms, cell cycle, metabolism and signaling. The first are oscillators based on cytoplasmic reactions, such as phosphorylation and oxidation. The second are genetic oscillators depending on gene expression regulation. In the last decade several synthetic genetic oscillators have been implemented in the laboratory. The first mathematical model of a genetic oscillator was developed by Goodwin for periodic enzyme production. This model was the groundwork for subsequent theoretical research on genetic oscillators in living systems, such as fungi and flies. In these models, the rhythms are generated by a gene with a negative transcriptional feedback. This NTF needs time delay and sufficiently strong nonlinearity in the transmission of the feedback signal for preventing the steady-state stabilization of the system. It has also been analyzed variants, involving two genes, of the model presented in the Fig. 1A. Positive transcriptional feedbacks are also present in many cellular clocks. Models with two or more genes involving PTFs have been studied in genetic oscillators. In these models the PTFs increase the expression of repressor genes. It has been shown how PTFs produce bistability, increase the robustness of cellular clocks and could provide robust adaptation to environmental cycles. Previously, it has been demonstrated that a single gene with only PTF does not produce oscillations. Here we study a model with a simple condition to produce biochemical rhythms in a single gene with PTF.