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The cancellation decision (hereafter, referred to as the braking process) is modeled as a latent competing signal, assumed to originate from the hyperdirect (brake) pathway and whose starting state depends on the state of the facilitation versus suppression competition.
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This dependency is largely consistent with the circuit-level architecture of corticobasal ganglia pathways where the direct (facilitation), indirect (suppression), and hyperdirect (brake) pathways converge at the primary output nucleus of the basal ganglia (i.e., the GPi in primates).
Because solvents acutely inhibit PFC output and impair cognitive processing, exposure to solvent vapor may have a multiplicative impact on the mesolimbic dopamine system, by (1) directly enhancing DA neuron activity, and (2) by removing a major brake on mesolimbic DA pathway output.
In mitochondria-dependent type 2 cells, IAPs such as survivin are major determinants of TRAIL-induced apoptosis, and it is thus plausible that inhibition of survivin would sensitize them to TRAIL-induced apoptosis by suppressing a brake on the mitochondrial pathway of apoptosis.
The factors governing the application of these brakes on the apoptotic pathway are currently unknown.
Alternatively, anti-inflammatory cytokines can be provided by administering recombinant protein, and intracellular "brakes" of inflammatory pathways can be introduced potentially by gene therapy.
CBL and LNK mutations inactivate brakes on signaling pathways and may have a dominant-negative effect.
The failure in these pathways (brakes) results in the pregnancy going out of control and the system crashing.
Lin, A. Activation of the JNK signaling pathway: breaking the brake on apoptosis.
Conversely, inactivation of this pathway releases the brake on adipogenesis [ 43- 45].
It is the failure in the braking systems, the endogenous protective pathway, that result in the 'accelerator' going out of control until the system crashes, manifesting itself as pre-eclampsia (http://youtube/vWUCWbKo1dE).
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