Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis

2007 ◽  
Vol 62 (7) ◽  
pp. 1044-1049 ◽  
Author(s):  
M. Czaja ◽  
A. Szarszewski ◽  
B. Kamińska ◽  
M. Bogotko-Szarszewska ◽  
G. Łuczak ◽  
...  
1999 ◽  
Vol 40 (4) ◽  
pp. 301 ◽  
Author(s):  
Jung Hwan Kim ◽  
Hyo Jin Park ◽  
Jun Sik Cho ◽  
Kwi Soon Lee ◽  
Sang In Lee ◽  
...  

2009 ◽  
Vol 207 (1-6) ◽  
pp. 85-87 ◽  
Author(s):  
H. E. Nielsen ◽  
C. K. Christensen ◽  
M. Brandsborg ◽  
O. Brandsborg

1973 ◽  
Vol 3 (3) ◽  
pp. 178-179 ◽  
Author(s):  
R. Håkanson ◽  
G. Liedberg ◽  
J. Oscarson ◽  
J. F. Rehfeld ◽  
F. Stadil

1981 ◽  
Vol 241 (3) ◽  
pp. G235-G241
Author(s):  
L. M. Lichtenberger ◽  
S. S. Crandell ◽  
P. A. Palma ◽  
F. H. Morriss

We investigated the perinatal ontogenic changes in ovine serum and tissue gastrin concentration. Fetal and maternal serum gastrin levels in serums obtained from indwelling catheters in the fetal and maternal circulations and tissue gastrin levels were assessed by radioimmunoassay and immunohistochemistry. Fetal serum gastrin concentration was undetectable until the 107th day of gestation and significantly increased to levels surpassing maternal values. Neonatal serum hormone concentration continued to rise, reaching a peak during the 4th postnatal wk and decreasing after the 4th wk coincident with weaning. Maternal serum gastrin concentration did not vary during pregnancy and did not correlate with fetal serum gastrin levels. Fetal abomasal and duodenal gastrin concentrations and abomasal G-cell number increased in parallel with the developmental alterations in fetal serum hormone levels during gestation. The developmental increase in abomasal gastrin concentration was not associated with a shift in the molecular form of the hormone. These findings support the hypothesis that circulating gastrin in the fetus is of fetal origin.


1972 ◽  
Vol 17 (6) ◽  
pp. 523-526 ◽  
Author(s):  
G. Lanciault ◽  
A. Merritt ◽  
E. Rosato ◽  
C. Bonoma ◽  
F. P. Brooks

1980 ◽  
Vol 17 (2) ◽  
pp. 177-186 ◽  
Author(s):  
R. P. Happé ◽  
I. Van Der Gaag ◽  
C.B.H.W. Lamers ◽  
J. Van Toorenburg ◽  
J. F. Rehfeld ◽  
...  

The main clinical signs of three dogs with Zollinger-Ellison syndrome were vomiting, diarrhoea, poor appetite and weight loss. The diagnosis was confirmed by histological examination and by gastrin immunocytochemistry. Gastrin was extracted from pancreatic tumours of two dogs. Gastrin-component III predominated in one dog while gastrin-compo-nent II and gastrin-component III were demonstrated in almost equal amounts in the other dog. In one dog serum gastrin concentration was high. Postmortem examination revealed pancreatic tumours in all three dogs and metastases in the regional lymph nodes and liver in two. The pancreatic tumours contained three patterns of growth: solid, trabecular and acinar. Electron microscopy of liver metastases showed cells with secretory granules. In all three dogs there was an erosive oesophagitis and thick gastric mucosa caused mainly by glandular proliferation. Two dogs had erosions and ulcers in the duodenum, one also in the first part of the jejunum. Villous atrophy and cellular infiltration of the duodenal mucosa were found in all dogs.


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