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In case of the enigma of individual differences in antidepressant response, a mouse model focussing on extremes (i.e., good or early responder versus poor or non-responder) in response to treatment with the most commonly prescribed antidepressant compounds, that is, serotonin reuptake inhibitors and serotonine-norepinephrine reuptake inhibitors, could be considered a straightforward approach.
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Notably, in an experimental setup mimicking specific immunotherapy (SIT) of an established allergic immune response in a mouse model of allergic asthma, transcutaneous application of allergen without any adjuvant could downregulate the TH2 response, supposedly by induction of FoxP3+ regulatory T cells [61].
The objective of the study was to determine the effect of statins on lipopolysaccharide (LPS -induced infLPS -inducedsponse inflammatoryodel of presponseinth (PTB).
Although it would be interesting to develop methods to reduce basal metabolic rate in humans based on the response seen a mouse model, relevant qualitative as well as semiquantitative information on the benefits of therapeutic strategies could still be obtained using small mammals.
In preclinical studies, this herbal formula, which is derived from ingredients used in traditional Chinese medicine, proved extremely effective in turning off the allergic response in a mouse model of peanut allergy.
These data indicate that B. pertussis infection induces a Th1/Th17 immune response in a mouse model.
Indeed, systemic administration of TGFβ alleviates the inflammatory response in a mouse model of arthritis [51] and impaired TGFβ signaling during infection with E. coli enhanced peritoneal inflammation in a rat model [52].
The results are found in Figure 2. The 70% increase in the expression of the GAG protein in vitro translated into more than a five-fold difference in humoral immune response in a mouse model.
We investigated the impact of immune regulatory mechanisms involved in the modulation of the recently presented, CD8+ lymphocyte mediated immune response in a mouse model of oligodendropathy-induced inflammation (PLPtg-mutants).
We recently showed that the cytoplasmic domain of CD248 is important in facilitating an inflammatory response in a mouse model of arthritis.
We show that the presence of beclomethasone promotes H. influenzae persistence without influencing the host inflammatory response in a mouse model of acute infection.
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