Dose-Response: An International Journal: Volume 11, Issue 3
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2013-30-09
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Dose-Response Vol 11, no 3, Front Matter
(2013-09-01)
Dose-Response Vol 11, no 3, Table of Contents
(2013-09-01)
CHEMICALS AND HEALTH - THOUGHT FOR FOOD
(2013-09-01) Bast, Aalt; Hanekamp, Jaap C.
In our contribution we concisely question and answer some basic notions on food, health, and safety. We show that for some food components such as flavonoids, a whole range of small toxicological effects that have been uncovered the last decade on the whole confer benefits to human health. This development underlines the notion that health is adaptation with respect to the exposures humans experience when consuming food.
SYSTEMS CANCER BIOLOGY AND THE CONTROLLING MECHANISMS FOR THE J-SHAPED CANCER DOSE RESPONSE: TOWARDS RELAXING THE LNT HYPOTHESIS
(2013-09-01) Lou, In Chio; Zhao, Yuchao; Wu, Yingjie; Ricci, Paolo F.
The hormesis phenomena or J-shaped dose response have been accepted as a com- mon phenomenon regardless of the involved biological model, endpoint measured and chemical class/physical stressor. This paper first introduced a mathematical dose response model based on systems biology approach. It links molecular-level cell cycle checkpoint control information to clonal growth cancer model to predict the possible shapes of the dose response curves of Ionizing Radiation (IR) induced tumor transformation frequency. J-shaped dose response curves have been captured with consideration of cell cycle checkpoint control mechanisms. The simulation results indicate the shape of the dose response curve relates to the behavior of the saddle-node points of the model in the bifurcation diagram. A simplified version of the model in previous work of the authors was used mathematically to analyze behaviors relating to the saddle-node points for the J-shaped dose response curve. It indicates that low-linear energy transfer (LET) is more likely to have a J-shaped dose response curve. This result emphasizes the significance of systems biology approach, which encourages collaboration of multidiscipline of biologists, toxicologists and mathematicians, to illustrate complex cancer-related events, and confirm the biphasic dose-response at low doses.
TEMPERATURE, NOT FINE PARTICULATE MATTER (PM2.5), IS CAUSALLY ASSOCIATED WITH SHORT-TERM ACUTE DAILY MORTALITY RATES: RESULTS FROM ONE HUNDRED UNITED STATES CITIES
(2013-09-01) Cox, Tony; Popken, Douglas; Ricci, Paolo F.
Exposures to fine particulate matter (PM2.5) in air (C) have been suspected of con- tributing causally to increased acute (e.g., same-day or next-day) human mortality rates (R). We tested this causal hypothesis in 100 United States cities using the publicly available NMMAPS database. Although a significant, approximately linear, statistical C-R association exists in simple statistical models, closer analysis suggests that it is not causal. Surprisingly, conditioning on other variables that have been extensively considered in previous analyses (usually using splines or other smoothers to approximate their effects), such as month of the year and mean daily temperature, suggests that they create strong, nonlinear con- founding that explains the statistical association between PM2.5 and mortality rates in this data set. As this finding disagrees with conventional wisdom, we apply several different techniques to examine it. Conditional independence tests for potential causation, nonparametric classification tree analysis, Bayesian Model Averaging (BMA), and Granger- Sims causality testing, show no evidence that PM2.5 concentrations have any causal impact on increasing mortality rates. This apparent absence of a causal C-R relation, despite their statistical association, has potentially important implications for managing and communicating the uncertain health risks associated with, but not necessarily caused by, PM2.5 exposures.