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MeSH Review

Hyperplasia

 
 
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Disease relevance of Hyperplasia

 

Psychiatry related information on Hyperplasia

 

High impact information on Hyperplasia

  • Specific inflammatory/immune response mediators can activate mucin gene regulation and airway remodeling, including goblet cell hyperplasia (GCH) [9].
  • Different Trp53 shRNAs produced distinct phenotypes in vivo, ranging from benign lymphoid hyperplasias to highly disseminated lymphomas that paralleled Trp53-/- lymphomagenesis in the E(mu)-Myc mouse [10].
  • Unexpectedly, ablation of Notch1 results in epidermal and corneal hyperplasia followed by the development of skin tumors and facilitated chemical-induced skin carcinogenesis [11].
  • Pontin reduction phenocopies the cardiac hyperplasia of the lik mutation [12].
  • Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia [13].
 

Chemical compound and disease context of Hyperplasia

  • Finally, this investigation contradicts the speculation that the association between this cancer and estrogen use can be explained by swifter diagnosis for estrogen users, misclassification of estrogen-related hyperplasia or treatment of early symptoms of the tumor with estrogen [14].
  • Serum aldosterone fell significantly (P less than 0.025) from the basal level in the patients with idiopathic aldosteronism due to hyperplasia [15].
  • The deficit in the activities of the first two enzymes resulted in decreased cortisol synthesis with subsequent increased ACTH secretion and adrenocortical hyperplasia [16].
  • Regression of parathyroid hyperplasia by calcitriol-pulse therapy in patients on long-term dialysis [17].
  • Neonates who receive prostaglandin E1 at recommended doses for more than 120 hours should be closely monitored for evidence of antral hyperplasia [18].
 

Biological context of Hyperplasia

 

Anatomical context of Hyperplasia

 

Gene context of Hyperplasia

 

Analytical, diagnostic and therapeutic context of Hyperplasia

References

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