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To date, only two studies exist that reports on WNT signaling expression in developing human lung.
Translating these findings into the developing human lung, recent studies performed by Popova et al. display a downregulation in PDGF-Rα expression upon TGF-β treatment in lung mesenchymal-like cells (MSCs) obtained from BPD patients [16].
Zhang et al. performed quantitative PCR and in situ hybridization using a developing human lung and showed that messenger RNA (mRNA) expression of WNT2, WNT7B, FZD4, FZD7, LRP5, and LRP6 was restricted to the alveolar and bronchial epithelium in the human lungs at 7, 12, 17, and 21 weeks of gestation [46].
The developing human lung undergoes a well-described series of morphologic changes, each of which occurs within a discrete period of embryonic and fetal development.
Our sampling technique also precludes us from specifically ascertaining the direct effect of maternal vitamin D levels on the developing human lung.
The observation that hnRNP A2/B1 is over-expressed in human hepatitis tissues indicates that hnRNP A2/B1 is involved in the promotion of the hepatocarcinogenesis. hnRNP A2/B1 has been suggested to be an onco-developmental protein, it was found that within the developing human lung (from 20 weeks onward), hnRNP A2/B1 had the highest expression level in the epithelial cells.
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The objectives of this study were to examine pulmonary lymphatic distribution in developing human lungs from normal and diseased infant lung tissue, and, importantly, to quantify and compare the abundance of lymphatic microvasculature at the acinar level in infants with CLD versus controls.
The device leverages the Wyss Institute team's previously developed human lung small airway-on-a-chip model for inflammatory disorders.
Leveraging their previously developed human lung small airway-on-a-chip model for inflammatory disorders including COPD and asthma, the Wyss Institute's team led by Founding Director Donald Ingber, M.D., Ph.D., designed a smoking instrument that integrates with the airway chips and faithfully recapitulates smoking behavior with cells derived from healthy people and patients with COPD.
In conclusion, we have demonstrated that vitamin D genes are actively regulated in the developing human fetal lung and that a disproportionate number of these genes are differentially regulated in asthma.
Further analysis revealed the gene activity in the lung organoids resembles that of the lung of a developing human fetus, suggesting that lung organoids grown in the dish are not fully mature.
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