The biologic rationale for a breast cancer effect stems from a hypothesis described by Labreche and Goldberg that organic solvents such as PCE may act either directly as genotoxic agents or indirectly through their metabolites to increase the risk of breast cancer [ 15].
This therapy stemmed from a straightforward hypothesis to explain the disease pathogenesis, namely that progressive enlargement of glycogen-filled lysosomes would lead to lysosomal rupture and to release of glycogen and toxic substances into the cytosol., The assumption was that early treatment, initiated before lysosomal integrity was compromised, would reverse this pathogenic cascade.
The simplest form of regulatory principle stemming from this hypothesis is that a perturbation (or a response to a perturbation) may trigger a regulatory response beginning at the first neighbors of the affected node(s), as illustrated in our earlier analysis of metabolic networks [ 5].
Historically, many theories of addiction have stemmed from a "self-medication" hypothesis, wherein continued substance abuse occurs as an attempt to prevent or relieve the experience of these negative withdrawal symptoms (Markou et al. 1998).
Since all these premises are either physico-chemical or geological, it seemed worthwhile to focus here on the biological predictions stemming from this hypothesis.
As noted by Popper, predictions stemming from the tested hypothesis must be logically uncoupled from the premises on which the hypothesis had been based [ 109].
Experimental evidence for this hypothesis stems from a comparison of basilar papilla tuning in two populations of cricket frogs, with the population in the acoustically more challenging habitat having evolved a filter that better eliminates noise [3], [4].
The dual mechanism hypothesis stems from a computational study of the role of the cerebellum in generating learned timing (i.e. delay) in classical delay conditioning (Hong and Optican, 2008).
One hypothesis holds that PTSD stems from a memory that is too strong, burned into the brain by hormones released in times of stress.
These simulations mirror a behavior known as overflow metabolism [ 66], where E. coli, at high growth rates, moves away from the full oxidation of glucose through the TCA cycle and uses less ATP efficient pathways, releasing acetate instead of CO 2. Our simulations support the hypothesis that this behavior stems from a tradeoff between enzyme cost and energy yield [ 40].
A second reason stems from the hypothesis that the maternally derived DMR must be protected from remethylation during the first stages of embryo development [73].
