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Infected persons develop hyperplasia of the bile ducts.
It is noteworthy that transgenic mice that overexpress BAFF in lymphoid cells develop hyperplasia of mature B cells [ 8, 17, 18] or pSS-like pathology [ 19].
Runx3-null mice reportedly develop hyperplasia of the gastric mucosa through activation of cellular proliferation and suppression of apoptosis in epithelial cells (Li et al, 2002).
Further evidence for the important role of a fine-tuned SHH pathway activation in progenitor cell cycle regulation is provided by findings in transgenic, Shh-overexpressing mice that develop hyperplasia of the spinal cord and the VZ during embryogenesis [ 34].
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Pre-cancerous conditions included one female (#286) having squamous dysplasia with extensive keratinization at the transformation zone between the uterus and the cervix, a second female (#365) developed hyperplasia of the fallopian tube with endothelial atypia, while a third female (#436) developed low grade dysplasia of squamous epithelium with acute cervicitis.
Interestingly, virgin P-cadherin null female mice exhibit precocious differentiation of the mammary gland, and develop hyperplasia and dysplasia with age.
Hyperplasia was diagnosed in 4% of those with estradiol monotherapy and 0.5% in the group receiving drospirenone 2 mg, with an 0.007 probability of developing hyperplasia.
In fact, gastric mucosa of Runx3-null mice develops hyperplasia due to the stimulated proliferation and suppressed apoptosis of epithelial cells [3].
Results: Mice homozygous for the mutation developed gastric hyperplasia of the glandular epithelium with numerous cysts.
Heterozygous and homozygous mice developed diffuse hyperplasia of interstitial cells of Cajal in the digestive tract (from esophagus to large intestine) and GIST-like cecal tumor.
In murine models of allergic asthma, mice repeatedly exposed to allergens or IL-13 develop goblet cell hyperplasia of the airway epithelium [ 15- 17].
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