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There are several models in which the reproduction of the phase diagram is much better than in the TIP4P model, e.g., the six-site model and TIP5P/ice model.
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There are several mental models in which to fit blockchain, and I, too, believe considering it as the new internet is not a bad analogy.
where k ∈ N, τ : ℤ → ℤ and τ (n + ω) = τ (n), f (n + ω, u) = f (n, u) for any (n, u) ∈ ℤ × ℝ, ω ∈ ℕ. Difference equations have attracted the interest of many researchers in the last 20 years since they provided a natural description of several discrete models, in which the periodic solution problem is always a important topic, and the reader can consult [1 7] and the references therein.
The role of Y. pestis YopJ in pathogenesis was examined in several mouse models in which it was found to be dispensable for virulence.
Phenotypically, mammary tumors induced in the BK5.ATF3 model resemble tumors and dysplastic lesions that have been reported in several transgenic models in which components of the Wnt/β-catenin pathway are overexpressed and the pathway is thereby constitutively activated [22] [28].
In a previous study, similarities were noted between the histopathology of ATF3-induced mammary tumors and lesions described in several transgenic models in which the Wnt/β-catenin pathway is upregulated.
Endotoxin-induced PH produces biphasic increase in mean pulmonary artery pressure (MPAP) in several animal models, in which the early phase is acute and transient [ 4].
The squamous differentiation characteristic of ATF3-induced tumors is phenotypically exceedingly similar to tumors produced in several transgenic models in which the Wnt/β-catenin pathway is stimulated.
While there has been speculation that incretins may play a role in pancreatic duct cell proliferation [7 9] and varying results have been reported for markers of pancreatitis in several animal models in which rodents were exposed to such agents [10 12], to date a biologic mechanism for incretin-induced pancreatitis has not been identified in humans.
The gradual and progressive decline in stem cell function in humans is reflected in the results of several model systems in which GATA2 is required to maintain stem cell self-renewal capacity (Tsai & Orkin, 1997; Nottingham et al, 2007; de Pater et al, 2013).
A broad range of infectious and autoimmune diseases that involve IL-1β have been associated with inappropriate activation of the inflammasome [12, 14, 15], while in several other disease models in which IL-1β plays a crucial role, the inflammasome appears not to be involved [16, 17].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com