How Occam's razor guides human decision-making.

Occam's razor is the principle that, all else being equal, simpler explanations should be preferred over more complex ones. This principle is thought to play a role in human perception and decision-making, but the nature of our presumed preference for simplicity is not understood. Here we use preregistered behavioral experiments informed by formal theories of statistical model selection to show that, when faced with uncertain evidence, human subjects exhibit preferences for particular, theoretically grounded forms of simplicity of the alternative explanations. These forms of simplicity can be understood in terms of geometrical features of statistical models treated as manifolds in the space of the probability distributions, in particular their dimensionality, boundaries, volume, and curvature. The simplicity preferences driven by these features, which are also exhibited by artificial neural networks trained to optimize performance on comparable tasks, generally improve decision accuracy, because they minimize over-sensitivity to noisy observations (i.e., overfitting). However, unlike for artificial networks, for human subjects these preferences persist even when they are maladaptive with respect to the task training and instructions. Thus, these preferences are not simply transient optimizations for particular task conditions but rather a more general feature of human decision-making. Taken together, our results imply that principled notions of statistical model complexity have direct, quantitative relevance to human and machine decision-making and establish a new understanding of the computational foundations, and behavioral benefits, of our predilection for inferring simplicity in the latent properties of our complex world.

Synchronization of dehydration and phosphorous immobilization for river sediment by calcified polyferric sulfate pretreatment.

Disposal of dredged river sediment requires decreases in both water content for reduction in disposal area, and the amount of eutrophication pollutants at risking of leaching. The effects of CaCl2, polyferric sulfate (PFS) and calcified polyferric sulfate (CaPFS) on dewatering and phosphorus immobilization were examined. Upon CaPFS dosage of 1.88 mg Ca + Fe kg-1 raw sediment (RS) the moisture content of the sediment was 41.1 wt% after pressure filtration, with filtrate dissolved inorganic phosphorus (DIP) of 6.1 mg L-1; better outcomes than for equivalent dosages of CaCl2 or PFS. On CaPFS dosage of 4.98 mg Ca + Fe kg-1 RS, DIP in the filtrate was <0.5 mg L-1. Dosages of CaCl2 and PFS required to achieve <0.5 mg L-1 DIP were 6.79 mg Ca kg-1 RS and 5.64 mg Fe kg-1 RS. CaPFS aids particle surface charge neutralization and sweep flocculation by polymeric iron, improving dehydration efficiency. Synergistic effects of aqueous Ca and Fe promote P stability reducing DIP mobility. For treatment of 10000 m3 of this dredged sediment, CaPFS has the potential to reduce the discharge of eutrophicated water by 74 ± 6% compared with PAC + PAM conditioning, demonstrating the promising application of CaPFS conditioning.

Protosappanin B promotes apoptosis and causes G1 cell cycle arrest in human bladder cancer cells.

The aim of the study was to investigate the effects of protosappanin B on the proliferation and apoptosis of bladder cancer cells. The effects of protosappanin B (12.5, 25, 50, 100, or 200 µg/mL, 48 h) on proliferation of SV-HUC-1, T24 and 5637 cells was assessed using the MTT assay. The effects of protosappanin B (100, 150, 200, 250, or 300 µg/mL, 48 h) on cell apoptosis and cell cycle were analyzed using flow cytometry. T24 and 5637 cells treated with 200 µg/mL protosappanin B showed morphological changes (shrinkage, rounding, membrane abnormalities, and reduced adhesion), but protosappanin B had no proliferation arrest effect on SV-HUC-1 cells. Protosappanin B caused concentration-dependent inhibition of cell growth, with IC50 of 82.78 µg/mL in T24 cells and 113.79 µg/mL in 5637 cells. Protosappanin B caused concentration-dependent increases in T24 and 5637 cell apoptosis (100-300 µg/mL). The effects of protosappanin B on the cell cycle in both cell types was G1 arrest with reductions in the proportion of S-phase cells and proliferation index. A proteomics analysis showed that protosappanin B modulated a number of genes involved in the cell cycle. In conclusion, protosappanin B inhibits the proliferation and promotes the apoptosis of T24 and 5637 human bladder cancer cells in a concentration-dependent manner, possibly via interference with cell cycle regulation, preventing G1-to-S transition.