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Based on these findings in mice, we hypothesized that insulin detemir might restore the decreased cerebral insulin response in overweight human subjects.
Given the baseline hypertrophy in miR-499-transgenic mice, we hypothesized that miR-499 expression may alter genes important in this cellular program, either directly or indirectly.
Given the massive neutrophil influx into the airways of B6.RAG-2γc−/− mice, we hypothesized that under these conditions neutrophils may contribute to pathology and disease.
Based on our observations of reduced αB-crystallin in older transgenic but not in non-transgenic mice, we hypothesized that if this chaperone is protective, then its loss may show an exaggerated phenotype.
Since we saw increased numbers of T cells in the lungs of FtDKO mice, we hypothesized that similar to CCR7-/ mice, FtDKO mice may show evidence of neo-lymphoid follicles or induced bronchus-associated lymphoid tissue (iBALT) in the lungs [26].
Since the salivary transcriptome was clearly altered in tumor-bearing vs. control mice, we hypothesized that the tumors behave like endocrine organs in that they secrete mediators (hormones, lymphokines, cytokines) which can affect the activity of TF in salivary glands and thereby induce up or down-regulation of transcripts levels in saliva.
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Because the inflammatory conditions were sporadically developed in the double mutant TNFR1KO/TAK1IEKO mice, we hypothesize that epithelial TAK1 signaling is important for preventing stress-induced barrier dysfunction.
Since FGF21 and FGF19v show very similar anti-diabetic effects in ob/ob mice, we hypothesize that commonly regulated pathways may contribute to their anti-diabetic effects.
Since there is no evidence of the vaccine candidate reaching the new born mice, we hypothesize that it may be due to trans-colostral transfer of protective anti-Salmonella antibodies.
Since, we have recently published [6] that a significant increase (5 fold) in bax mRNA transcript and protein occurs in oocytes of aged ICR mice, we hypothesize that Bax is most probably involved in setting the slower rate of repair observed in oocytes of aged ICR mice.
As one potential explanation for the tumor latency differences between the p53−/− and 3 month p53 deleted mice, we hypothesize that p53 has a significant protective effect on genomic integrity during embryogenesis and early postnatal development, when cell division rates are high and prone to potential chromosomal abnormalities.
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