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Gallamine despite having low bulk and rigidity is the most potent in its class, and it measures 1.9 nm. [6] [19] Based on this information one can conclude that the optimum length for neuromuscular blocking agents, depolarizing or not, should be 2 to 2.1 nm. [20]
Potassium channel blockers exhibit reverse use-dependent prolongation of the action potential duration. Reverse use dependence is the effect where the efficacy of the drug is reduced after repeated use of the tissue. [ 11 ]
PD-1/PD-L1 blockade therapy is not effective for all patients, as some may exhibit resistance. To overcome resistance, a strategy involving the combination of PD-1/PD-L1 inhibitors with type I interferons has emerged. The combination of PD-1/PD-L1 inhibitors and type I interferons has shown promise in preclinical and clinical studies (phases I ...
Some research is devoted to finding combinations of extant antibiotics which when combined exhibit synergy. A classic example of this effect is the interaction between β-lactams, which damage the bacteria cell membrane, and aminoglycosides, which inhibit protein synthesis. [1]
Histone deacetylase inhibitors may modulate the latency of some viruses, resulting in reactivation. [41] This has been shown to occur, for instance, with a latent human herpesvirus-6 infection. Histone deacetylase inhibitors have shown activity against certain Plasmodium species and stages which may indicate they have potential in malaria ...
Irreversible inhibitors covalently bind to an enzyme, and this type of inhibition can therefore not be readily reversed. [51] Irreversible inhibitors often contain reactive functional groups such as nitrogen mustards, aldehydes, haloalkanes, alkenes, Michael acceptors, phenyl sulfonates, or fluorophosphonates. [52]
Untransformed human cells exhibit normal cellular behavior and mediate their growth and proliferation via interplay between environmental nutrients, growth factor signaling, and cell density. As cell density increases and the culture becomes confluent, they initiate cell cycle arrest and downregulate proliferation and mitogen signaling pathways ...
a possible mechanism of non-competitive inhibition, a kind of mixed inhibition.. Mixed inhibition is a type of enzyme inhibition in which the inhibitor may bind to the enzyme whether or not the enzyme has already bound the substrate but has a greater affinity for one state or the other. [1]