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Interestingly, ghrelin levels in AN are markedly increased, supporting the concept that in chronic food restriction (and probably in AN), a dysregulation of the agouti-related protein (AgRP) system contributes to deficient ghrelin signaling at the level of the ARC [ 19].
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Abnormal response monitoring may also contribute to deficient cognitive control of behaviour in ASD, which, in the present study, was reflected in an increased antisaccade error rate, consistent with prior work (Manoach et al., 1997, 2004; Minshew et al., 1999; Goldberg et al., 2002; Luna et al., 2007) and possibly in reduced dynamic performance adjustment.
Impairment of this function may contribute to deficient performance in more complex allocentric memory tasks.
Several mechanisms could contribute to deficient processing, such as decreased voluntary attention [38], reduced voluntary rehearsal [39], and short-term perceptual priming [40].
Pathologic examination of the placenta can yield important clues to factors contributing to deficient fetal growth.
In addition, the hippocampal and prefrontal deficits observed in persons with anxiety disorders such as posttraumatic stress disorder suggest that the acquisition of contextual information might be impaired and that this might contribute to deficient cue extinction as previously shown (Orr et al., 2000; Wessa & Flor, 2007).
Therefore, in conclusion, enhanced autophagy in epithelial cells has a deleterious effect by promoting cell death and developing of emphysema, and impaired autophagy in alveolar macrophages contributes to the deficient transport of bacteria to lysosome, namely, xenophagy, and to the higher propensity of COPD patients to bacterial acute respiratory infections which lead to acute exacerbations.
Performance on free recall in this group is significantly predicted by scores on executive tests, indicating that executive dysfunction contributes to retrieval failure (deficient internal search strategies), and is responsible for the apparent mnemonic deficit rather than a dysfunction of storage (Pillon et al., 1993; Costa et al., 2014).
Potentially, this oscillatory pattern of Ca2+ signalling may be less able to stimulate NO formation and contribute to the deficient relaxatory response observed, though this, and the relation to decreased SOCE, remains speculative.
Although further studies are needed to substantiate the functional significance of the glymphatic concept, one implication is that glymphatic pathway dysfunction may contribute to the deficient amyloid-β clearance in Alzheimer's disease.
Although these concepts are also challenged and further studies are needed to substantiate their functional significance [ 1], one implication is that glymphatic pathway dysfunction may contribute to the deficient Aβ clearance in the pre-clinical stages of Alzheimer's disease (AD) [ 5].
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