scholarly journals Decreased Gastric Gland Mucin-specific O-glycans Are Involved in the Progression of Ovarian Primary Mucinous Tumours

2021 ◽  
Author(s):  
Ayumi Ohya ◽  
Hisanori Matoba ◽  
Yasunari Fujinaga ◽  
Jun Nakayama
Keyword(s):  
Gastric Gland ◽  
Mucinous Tumours

scholarly journals Regulation of free cytosolic Ca2+ in the peptic and parietal cells of the rabbit gastric gland.

1986 ◽  
Vol 261 (6) ◽  
pp. 2660-2667
Author(s):  
S Muallem ◽  
C J Fimmel ◽  
S J Pandol ◽  
G Sachs
Keyword(s):  
Gastric Gland ◽  
Parietal Cells

scholarly journals Aspects of the biology of regeneration and repair in the human gastrointestinal tract

1998 ◽  
Vol 353 (1370) ◽  
pp. 925-933 ◽  
Author(s):  
Nicholas A. Wright
Keyword(s):  
Stem Cells ◽  
Gastric Gland ◽  
Cell Lineage ◽  
Mucosal Ulceration ◽  
Cell Lineages ◽  
Trefoil Peptides ◽  
Pyloric Mucosa ◽  
A Cell ◽  
Epidermal Growth ◽  
Altered Gene

The main pathways of epithelial differentiation in the intestine, Paneth, mucous, endocrine and columnar cell lineages are well recognized. However, in abnormal circumstances, for example in mucosal ulceration, a cell lineage with features distinct from these emerges, which has often been dismissed in the past as ‘pyloric’ metaplasia, because of its morphological resemblance to the pyloric mucosa in the stomach. However, we can conclude that this cell lineage has a defined phenotype unique in gastrointestinal epithelia, has a histogenesis that resembles that of Brunner's glands, but acquires a proliferative organization similar to that of the gastric gland. It expresses several peptides of particular interest, including epidermal growth factor, the trefoil peptides TFF1, TFF2, TFF3, lysozyme and PSTI. The presence of this lineage also appears to cause altered gene expression in adjacent indigenous cell lineages. We propose that this cell lineage is induced in gastrointestinal stem cells as a result of chronic mucosal ulceration, and plays an important part in ulcer healing; it should therefore be added to the repertoire of gastrointestinal stem cells.

scholarly journals Role of CA 19-9 in complex ovarian tumors

2016 ◽  
Author(s):  
Dhanya S. Thomas ◽  
Ajit Sebastian ◽  
Vinotha Thomas ◽  
Anitha Thomas ◽  
Rachel Chandy ◽  
...  
Keyword(s):  
Malignant Tumors ◽  
Ovarian Tumors ◽  
Benign Tumors ◽  
Ovarian Mass ◽  
Radiological Findings ◽  
Epithelial Tumors ◽  
Mucin Glycoprotein ◽  
Glycoprotein Antigen ◽  
Mucinous Tumours

Background: Cancer antigen 19-9 (CA 19-9) is a tumor-associated mucin glycoprotein antigen that may be elevated in healthy individuals as well as in patients with benign and malignant tumors. It is useful in the management of pancreatic and other gastrointestinal tumors. CA 19-9 is also elevated in benign and malignant ovarian tumors. Aim: To study the pattern of serum CA19-9 in complex ovarian tumors. Methods: The study design was descriptive, based on data collected from medical records. Patients with a complex ovarian mass, who were investigated with CA 19-9 and had undergone surgery, wereincluded in the study. The study duration was 2 years from January 2014 to December 2015. A total of 273 patients (119 - benign and 154 malignant) with complex ovarian mass and elevated CA 19-9 underwent surgery during the study period. Results: CA 19-9 was elevated in 55 patients (20%). Of these, 23 patients had benign tumors while 32 had malignant tumors.Among patients with benign tumors, 21 had dermoid, 23 had mucinous tumors and 75 had other types of tumors. CA 19-9 was elevated in 10 (47.6%) of the dermoids, 7 (30.4%) of the mucinous tumors and 6 (8%) of the other benign tumors. Among patients with malignant tumors, 138 were epithelial and 16 were non epithelial tumors. Of the epithelial tumors, 31 were mucinous and 107 were non mucinous types. Overall, 29 (21%) had elevated CA 19-9. Of the epithelial tumors, 22.6% of the mucinous type and 20.6% of the non mucinous type had elevated CA 19-9. Among the non-epithelial tumors, 3 (18.8%) had elevated CA19-9. Conclusion: CA 19-9 is elevated in several conditions but most likely to be raised in dermoid cysts and mucinous tumours. CA19-9 levels need to be interpreted along with clinical and radiological findings.

A Model of the Gastric Gland Ejection Cycle: Low Ejection Fractions Require Reduction of the Glandular Dead Space

2001 ◽  
Vol 210 (3) ◽  
pp. 337-343
Author(s):  
SVEN KURBEL ◽  
BEATRICA KURBEL ◽  
BRANKO DMITROVIĆ ◽  
ALEKSANDAR VČEV
Keyword(s):  
Dead Space ◽  
Gastric Gland

Progressive genomic alterations in intraductal papillary mucinous tumours of the pancreas and morphologically similar lesions of the pancreatic ducts

2003 ◽  
Vol 199 (4) ◽  
pp. 453-461 ◽  
Author(s):  
Davide Soldini ◽  
Matthias Gugger ◽  
Elisabeth Burckhardt ◽  
Andreas Kappeler ◽  
Jean A Laissue ◽  
...  
Keyword(s):  
Pancreatic Ducts ◽  
Genomic Alterations ◽  
Mucinous Tumours

The ulceration-associated cell lineage (UACL) reiterates the Brunner's gland differentiation programme but acquires the proliferative organization of the gastric gland

1994 ◽  
Vol 173 (4) ◽  
pp. 317-326 ◽  
Author(s):  
Dennis J. Ahnen ◽  
Richard Poulsom ◽  
Gordon W. H. Stamp ◽  
George Elia ◽  
Christine Pike ◽  
...  
Keyword(s):  
Gastric Gland ◽  
Cell Lineage ◽  
Brunner’S Gland ◽  
Brunner's Gland

Inhibition of acid secretion in isolated gastric glands by substituted benzimidazoles

1982 ◽  
Vol 243 (6) ◽  
pp. G505-G510 ◽  
Author(s):  
E. Fellenius ◽  
B. Elander ◽  
B. Wallmark ◽  
H. F. Helander ◽  
T. Berglindh
Keyword(s):  
Oxygen Consumption ◽  
Gastric Gland ◽  
Acid Formation ◽  
Gastric Glands ◽  
New Class ◽  
Weak Bases ◽  
Morphological Studies ◽  
Isolated Gastric Glands ◽  
Dose Dependent ◽  
Distal Site

A new class of gastric acid inhibitors, substituted benzimidazoles (H 83/69 and H 149/94), have been tested in an isolated rabbit gastric gland preparation. Acid formation in the glands was stimulated by histamine, dibutyryl cAMP (DBcAMP), and high extracellular K+ concentrations, and the glandular secretory response was measured by changes in oxygen consumption and in accumulation of the weak base [14C]aminopyrine (AP). The substituted benzimidazoles inhibited AP accumulation induced by all stimulants in a dose-dependent noncompetitive manner. In contrast, cimetidine only inhibited histamine-induced AP accumulation. Basal AP accumulation, not affected by cimetidine, was also inhibited by the substituted benzimidazoles, as was the increase in glandular oxygen consumption produced by the addition of histamine and DBcAMP. Basal oxygen consumption was inhibited by about 15%. The substituted benzimidazoles, like AP, are weak bases and were also found to accumulate in the glands. Semiquantitative morphological studies of glands stimulated by histamine plus theophylline did not show any change in the enlarged secretory surface area after stimulation in the presence of inhibitory concentrations of H 149/94 (10(-4) M). The results suggest that substituted benzimidazoles have a mechanism of action different from that of H2-receptor antagonists and indicate a very distal site of action in the events leading to acid formation.

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