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The planning model, therefore, features a process-specific degeneration effect that penalizes if the organization focuses too much on distinct processes or the BPM capability.
Otherwise, the relative effect on quality equals η i. (eta_{i} in ]0;1]) is the process-specific quality degeneration effect (q_{i}^{ hbox{max} } in {mathbb{R}}^) is the process-specific upper quality boundary.
Project (5), in contrast, is not included in the optimal project roadmap as the critical time boundary of process (III) is never violated due to the low degeneration effect and the good time-performance at the decision point.
Analogous to quality, the planning model incorporates a process-specific degeneration effect that occurs whenever the organization does not conduct a process-level project regarding the process at hand.
Otherwise, the absolute effect on time equals 0. (beta_{i,y - 1}^{{{text{rel}}.}} in ]0;infty [) is the relative effect on quality, equals (beta_{s}^{{{text{rel}}.}}) if a process-level project (s in S) with respect to process i has been finished in period y – 1. Otherwise, the relative effect on time equals θ i. (theta_{i} in [1;infty [) is the process-specific time degeneration effect.
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After careful deliberation and additional literature work, we included selected comments (e.g., additional interactions types, degeneration effects on selected performance dimensions) in the design specification as shown in Sect.
Here, we show that myostatin inhibition by follistatin transgene expression in Dysf −/− mice results in early improvement in histopathology but ultimately exacerbates muscle degeneration; this effect was not observed in dystrophin-deficient (mdx) mice, suggesting that accelerated degeneration induced by follistatin transgene expression is specific to mice lacking dysferlin.
In retinas compromised by degeneration, the effects of this detachment would only be further magnified [18].
While expression of human α-synuclein in C. elegans results in dopaminergic neuron degeneration, the effects of α-synuclein on dopamine homeostasis and its contribution to dopaminergic neuron degeneration in C. elegans have not been reported.
A Phase I clinical trial identified that PEDF had therapeutic effects in wet age-related macular degeneration, and the effect of PEDF as an anti-angiogenic agent in this model was promising [ 242].
Transplantation of astrocytes expressing tyrosine hydroxylase (TH) and/or BDNF blocked 6-OHDA-induced degeneration and the effect of TH plus BDNF was more effective than either alone [ 87].
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