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Thus, we hypothesized expression differences of endothelin-1, TGF- β1, TGF- β2, and TGF- β3, of their receptors T βRI, T βRII, and of their pseudoreceptor BAMBI in lung tissue of broilers with ascites, with right cardiac failure but without ascites and in healthy broilers.
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Next, we hypothesized that expression differences of anchor genes would cause expression differences (in trans) on multiple downstream genes (targets).
We hypothesized that expression that is concordant across tissues is more likely influenced by genetic variability than gene expression which is discordant between tissues.
As hypothesized, monoallelic expression of IGF2 was observed in MSC population 4 (figure 4 and figure S2) whereas bi-allelic expression was observed in population 1 (figure S2).
We hypothesized that expression of HIV-1 Tat protein in a rodent model would potentiate the behavioral psychostimulant response to cocaine.
Given this ability to export O., we hypothesized that expression of AE2 in the lung is regulated by oxidative stress.
Specifically we hypothesized that expression of the neurotrophins and their cognate receptors is increased by dieldrin exposure.
We hypothesized that expression of these cell cycle genes in DP thymocytes might contribute to their inherent sensitivity to apoptosis.
We hypothesized the expression of these interactors would be good barometers for change under sub-lethal (10 nM) rotenone treatment.
Based on these findings, we had hypothesized that expression of pseudorabies IE180 would cause the developmental neurological abnormalities in host animals without viral infection and replication.
Therefore, we hypothesized that expression of activin βA, activin RIIB, or follistatin may be modulated in response to FAD exposure.
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