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Second, McCrea, Liberman, Trope and Sherman (2008) found that manipulating level of goal/action identification causally influenced extent of procrastination.
First, experimentally manipulating level of goal/action identification influences emotional response to a subsequent anagram stress failure task (Moberly & Watkins, 2006; Watkins et al., 2008).
Third, experimentally manipulating level of goal/action identification influences emotional response to a subsequent stress failure task (Moberly & Watkins, 2006; Watkins et al., 2008), with more concrete identifications resulting in less emotional reactivity.
This conclusion was based on evidence that: (i) unhelpful RT is characterized by an abstract level of processing and (ii) manipulating level of goal/action identification influenced the consequences of RT (see Watkins, 2008).
Moreover, any evidence that manipulating level of goal/action identification influences clinically-relevant outcomes, such as symptoms and processes involved in psychological disorders, would suggest that impaired regulation of level of goal/action identification may potentially be involved in the onset and maintenance of psychopathology.
However, a number of experimental studies have shown that manipulating level of goal/action identification causally influences self-control on a range of experimental tasks, with more abstract level of identification producing greater resistance to temptation than more concrete level of identification (Fujita & Han, 2009; Fujita et al., 2006; Schmeichel & Vohs, 2009).
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Drosophila copper tolerance can be altered by manipulating levels of known copper uptake proteins or metallothioneins directly or via suppression of the metallothionein transcription factor, MTF-1 [13], [31], [31].
Moreover, origin specificity can be achieved by manipulating levels of ORC and competitor DNA.
Furthermore, resistance to this synthetic retinoid can be overcome by manipulating levels of cytotoxic SLs, creating opportunities for other alternative treatments.
We then tested the hypothesis that the mechanism for these observations is due to the effect of these chemotactic factors on OPC migration and subsequent remyelination by manipulating levels of Sema3A or 3F in a mouse model of demyelination.
While manipulating levels of genetic variance is an attractive approach to test general predictions, we also need to carry out experiments with natural populations that capture effective standing genetic variation in the wild.
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