The MT evaluation examined subepithelial collagen thickness,
goblet cell count, and subepithelial fibrosis.
Although no obvious gross pathologic changes were attributed to the nematode, histologic changes of bronchial epithelial hyperplasia and
goblet cell metaplasia, consistent with chronic airway irritation were found in the lungs associated with Diplotriaena eggs.
Finisher phase,
Goblet cell count, Growth performance, Lymphoid organs, MOS.
MUC2 is a highly specific marker of
goblet cell metaplasia in the distal esophagus and gastroesophageal junction.
B and C, Mucinous adenocarcinoma, intestinal type with
goblet cell differentiation, sometimes associated with extravasated mucin imparting a colloid-like appearance.
Both the Gln and Arg affected the
goblet cell number (GCN) in duodenum (p<0.05) and the 0.5% Gln+130% Arg and 1.0% Gln+ 160% Arg fed birds had higher GCN.
Tissue samples taken from the upper and lower conjunctiva and lacrimal gland were stained with hematoxylin and eosin and periodic acid-Schiff and evaluated in terms of inflammatory cell density and
goblet cell numbers.
Since carcinoid tumor was first described by Merling (2) in 1838, three different histological subtypes have been described: argentaffin-positive carcinoid; non-argentaffin carcinoid; and
goblet cell carcinoid (GCC) (3).
From the AB-PAS staining, the normal control group showed rare
goblet cells and no mucus secretion, and the asthmatic model group had more
goblet cell hyperplasia in airway epithelia and more mucus secretion (Figure 4A and B).
Previous studies have shown that there are some wound-healing events in asthmatic airways, which were characterized by mucosa epithelial apoptosis/erosion,
goblet cell hyperplasia/hypertrophy, thickening of basement membrane, epithelial fibrosis, submucosal gland hyperplasia, mucus secretion, hyperplasia of smooth muscle hypertrophy, hyperplasia of blood vessels, etc.[11],[12] Studies on the abnormal injury and repair of upper airway allergic diseases are relatively scarce.
The retrospective study found that appendix cancer is comprised of five distinct subtypes- mucinous adenocarcinomas (46 percent), adenocarcinomas (30 percent),
goblet cell carcinoids (12 percent), pseudomyxoma peritonei (7.7 percent) and signet ring cell carcinomas (5.2 percent).
They demonstrated that Notch inhibition could induce
goblet cell differentiation and reduce cell proliferation, while cellular proliferation and progression of BE could be promoted by Notch activation, suggesting that Notch signaling might play binary roles in regulating Barrett metaplasia and its progression [4].