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With regard to the comparison between cyclophosphamide and CyA, we could not make a definitive conclusion, as the doses of steroid concurrently used with these agents were different.
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A natural response to this argument is that if the environments of the two agents are different, and this is responsible for their semantic divergence, then that environmental difference simply needs to be folded into the relevant laws, which are of course massively underdescribed anyway (clearly more than P1 by itself is needed to guarantee any effect, and thus M1).
However, total wealth of agents is different between the tax and the no-tax economy.
It is possible that the binding kinetics (association and dissociation rates) among these anti-TNF-α agents are different.
However, binding affinities of the agents are different.
Available agents are different kinds of gadolinium ion based chelates which are relatively stable molecules.
However, the pharmacokinetics and binding profiles of these agents are different [ 1].
Management of infections by these agents is different from that of tuberculosis.
Although the primary intracellular targets –of action of chemotherapy agents are different, it has become evident that induced cytotoxicity converges, ultimately, on a common pathway that induces apoptosis.
Although the mechanism of action of adalimumab and other anti-TNF agents is not completely understood, it is clear that the biological effects of these agents are different from those of DMARDs.
However, capecitabine and S-1 are of different drug designs and it has been reported that predictive factors for the efficacy of these two agents are different [ 13, 14].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com