Search PubMed⌕ Search

Biomedical subjects

G Pals

Publications and source records attributed to G Pals.

At least 109 records · Page 6Linked to original sources
PubMed1986

Effect of single and repeated doses of oral omeprazole on gastric acid and pepsin secretion and fasting serum gastrin and serum pepsinogen I levels.

The effect of omeprazole on gastric acid and pepsin secretion and fasting serum gastrin and serum pepsinogen I levels was studied in 12 healthy volunteers. Omeprazole, 40 mg enteric-coated granules, or placebo was given once daily for nine days in a double-blind crossover study design. Twenty-four hours after a single dose of omeprazole, mean basal and mean pentagastrin-stimulated acid output decreased significantly. This effect was more pronounced after nine days of treatment. Basal pepsin output was significantly reduced only in those subjects with basal anacidity during omeprazole treatment. Stimulated pepsin output was slightly reduced after a single dose but unaltered after nine days of omeprazole. Fasting serum gastrin and serum pepsinogen I levels increased significantly during omeprazole treatment. It is concluded that omeprazole is a potent and selective inhibitor of gastric acid secretion, probably without a direct effect on pepsin secretion. However, in cases of basal anacidity during omeprazole administration, basal pepsin secretion is reduced. During omeprazole treatment, fasting serum levels of gastrin and pepsinogen I rise.

Administration, Oral↗
PubMed1986

Pepsinogen A polymorphism in gastric mucosa and urine, with special reference to patients with gastric cancer.

Electrophoretic pepsinogen A patterns were determined in gastric fundic mucosa biopsies from 601 patients with various gastric disorders and 25 healthy volunteers. Pepsinogen A patterns with an intense fraction 5 appeared to be associated with gastric cancer and premalignant changes of the stomach (p less than 10(-9)). In 60 individuals pepsinogen A patterns were determined in normal mucosa from different parts of the stomach. No differences were found between these patterns. In 29 out of 59 gastric cancer patients pepsinogen A could be demonstrated in the macroscopically malignant tissue. In two cases a different pattern compared with uninvolved fundic mucosa was observed. During a follow up study, major changes in the pepsinogen A pattern were observed in 7 out of 56 patients. In 8.6% of the examined patients urinary pepsinogen A patterns differed considerably as compared with the pattern observed in the gastric fundus. The results suggest that the highly significant association between intense Pg5 (the product of the D gene) and gastric cancer or its precursors may be caused by genetic as well as non-genetic factors.

Gastric Fundus↗
PubMed1985

The influence of omeprazole on the synthesis and secretion of pepsinogen in isolated rabbit gastric glands.

Regulation mechanisms of pepsinogen (EC 3.4.23.) synthesis and secretion were studied by following newly synthesized [14C]-labeled pepsinogen during culture of isolated rabbit gastric glands. Omeprazole, a substituted benzimidazole, while almost completely abolishing acid production at 10(-4) M, strongly stimulated secretion of preformed and newly synthesized pepsinogen. Although the pepsinogen synthesis at this concentration of omeprazole was reduced to about 55% of the control rate, a two-fold absolute increase of total secreted pepsinogen was found. This increase was not due to a non specific leakage through disruption of chief cell membranes, as no increase of lactate dehydrogenase in the culture medium could be demonstrated. The stimulated secretion was influenced neither by 10(-3) M cimetidine, 10(-3) sodium thiocyanate nor 10(-4) M atropine. No additivity was found between the carbachol (10(-4) M) or dibutyryl cyclic AMP (10(-3) M) and the omeprazole induced pepsinogen secretion.

Animals↗
PubMed1985

Influence of RP 40749 on basal and meal-stimulated serum-gastrin, serum-pepsinogen I, and gastrin-content of the antral mucosa in duodenal ulcer patients.

Eighteen patients with active duodenal ulcer were treated with a novel antisecretory drug, RP 40749, either 100 mg or 150 mg as a daily nocturnal dose for 28 days. In these patients we evaluated the clinical course, endoscopic healing rates after 28 days, routine laboratory parameters, basal serum gastrin and pepsinogen I levels, meal-stimulated serum gastrin concentration, and the gastrin content of the antral mucosa. All nine patients receiving 150 mg RP 40749 and eight of nine patients receiving 100 mg RP 40749 healed their ulcers completely within 28 days, becoming rapidly symptom-free after an average of three days. The basal (53.8 +/- 5.2 vs 99.8 +/- 11.4 pg/ml) and meal-stimulated serum gastrin levels (109.2 +/- 12.1 vs 189.2 +/- 16.7 pg/ml) rose significantly after treatment with RP 40749, as did the gastrin content of the antral mucosa (11.3 +/- 2.1 vs 26.0 +/- 5.1 micrograms/g), suggesting increased synthesis and secretion of gastrin. Between the 100 mg and 150 mg groups, no significant differences in response were observed. Serum pepsinogen I levels (64.9 +/- 7.3 vs 147.9 +/- 17.9 ng/ml) increased after treatment; the increase after 150 mg RP 40749 was significantly greater than that after 100 mg RP 40749. The increase of serum pepsinogen levels are probably due to a spillover effect resulting from a blockade in exocrine secretion into the lumen. There were no relevant changes in routine laboratory parameters.

Adult↗
PubMed1985

Purification of the pepsinogen A isozymogens by means of high resolution ion-exchange chromatography. Evidence for post-translational modifications.

Total human pepsinogen (PG) was isolated from gastric fundic mucosa and PGA (formerly called PGI) from urine, using standard ion-exchange and gel filtration techniques. Gastric PGA was separated from PGC (formerly called PGII) either by immunoaffinity or high resolution ion-exchange chromatography (fast protein liquid chromatography, Pharmacia, Uppsala, Sweden). The individual PGA isozymogens 2, 3, 4 and 5 could be isolated to homogeneity with the aid of the same ion-exchanger. Evidence was obtained for the existence of secondary modifications of the PGA fractions 3, 4 and 5, electrophoretically overlapping the primary (genetic) isozymogens.

Chromatography, Gel↗
PubMed1985

Pepsinogen synthesis and secretion by isolated gastric glands.

De novo synthesis of pepsinogens was demonstrated in gastric glands isolated from rabbit and human gastric mucosa. The isolated glands were incubated in an amino acid free, Minimum Eagles Medium supplemented with a 14C labelled amino acid mixture. The glands were centrifuged at different time intervals and aliquots of gland homogenates and medium were run on polyacrylamide slab gels. Newly synthesized pepsinogens were demonstrated by autoradiography. Incorporation of 14C was detected after 30 minutes of culture and increased almost linearily with time over 4 h. By comparing the electrophoretic patterns after autoradiography, protein and pepsinogen activity staining, it was concluded that the glands synthesize mainly pepsinogens. Cimetidine, at a concentration of 10(-4)M strongly inhibited pepsinogen synthesis. Spontaneous secretion of pepsinogens into the medium was very low and relatively constant. Cyclic dibutyryl AMP markedly stimulated the secretion of pepsinogens into the medium. The results show, that isolated gastric glands are capable of synthesis and secretion of pepsinogens and that each function can be stimulated and inhibited selectively.

Animals↗
PubMed1985

Immunocytochemical localization of pepsinogen I and II in the human stomach.

An immunoperoxidase method using antisera specific for PG I and PG II was developed to assess PG-containing cells in the human stomach. Fundus-chief cells contained abundant PG I and less PG II. Mucus neck cells stained more frequently with anti-PG I, while antral gland cells stained only with anti-PG II. In adenocarcinoma of the corpus, isolated glands faintly staining with anti-PG I or anti-PG II were observed. In dense tumorous tissue no anti-PG I activity could be observed, while PG II sometimes remained present in residual antral glands, even in areas of heavy tumor infiltration. Focal PG II activity was also clearly demonstrated in some antral tumor cells. The immunoperoxidase technique described is suitable for further detailed studies of normal and pathological conditions of the gastric mucosa.

Adenocarcinoma↗
PubMed1985

Qualitative and quantitative determinations of pepsinogen I in gastric cancer and premalignant changes of the stomach.

Previous studies in rats have shown that stomach carcinogens cause a decrease of total pepsinogen content and a decrease of the fastest pepsinogen isozymogen in gastric mucosa before the appearance of carcinoma. In man the presence of Pg 5, and in particular a strong Pg 5, appears to be associated with gastric cancer. Low serum PG I levels were found in patients with gastric cancer, atrophic gastritis, intestinal metaplasia and gastric polyp. In this chapter we review the literature and report our results of PG I isozymogen and serum PG I determinations in 500 patients with various gastric disorders. It is concluded that premalignant changes of the stomach are associated with the presence of a strong Pg 5 isozymogen and with a low serum PG I level.

Gastritis, Atrophic↗
PubMed1985

Serum pepsinogen I levels: assessment of gastric acid secretion?

We measured serum PG I levels by an Elisa technique before and after stimulation with pentagastrin in 260 patients (161 males and 99 females). The serum levels were correlated to basic acid output (BAO), maximum acid output (MAO) and peak acid output (PAO). The correlation coefficient between serum PG I and PAO varied between -0.482 and 0.744 depending on the diagnosis. This indicates that a simple measurement of PG I cannot replace the pentagastrin test in estimating gastric acid secreting capacity. However, since all patients who were achlorhydric had a serum PG I level of less than 50 micrograms/l the measurement of serum PG I can be recommended as a screening test for achlorhydria.

Achlorhydria↗
PubMed1985

Serum pepsinogen I levels in relation to pepsinogen phenotypes.

Serum PG I levels were measured by an enzyme linked immuno sorbent assay (ELISA) in 567 blood donors and 171 patients from a routine gastroscopy program to study the relationship between PG I phenotypes and serum levels. In normal subjects no association was found between PG I phenotypes and serum levels. A low serum PG I level in patients was associated with phenotypes characterized by intense PG I fraction 5. This probably reflects the high frequency of these phenotypes in patients with atrophic gastritis or gastric cancer. The mean (+/- SD) serum PG I level was 45.8 +/- 17.7 micrograms/1 in control subjects. Serum PG I levels were lower in females (41.4 +/- 17.5) than in males (47.3 +/- 17.7) and increased with advancing age up to 65 years.

Adolescent↗
PubMed1984

Genetics of urinary pepsinogen: a new hypothesis.

A new genetic model is proposed to explain the inheritance of the urinary pepsinogen (PG1) polymorphism. Each main fraction, 3, 4 and 5, in the multibanded electrophoretic pattern, is determined by its own specific gene, B, C and D respectively. The intensity ratio of the fractions is principally determined by the number of gene copies. Accordingly, the PG1 phenotypes are determined by gene combinations, haplotypes, some of which may be identical to alleles in previous one locus models. Some critical families, not interpretable using previous genetic models, are presented to support the hypothesis. Preliminary population data from the Netherlands are described. The molecular background of this polymorphism and its relevance for gastric (pre)malignancy is discussed.

Adult↗
PubMed1984

Pepsinogen synthesis and secretion in isolated gastric glands.

De novo synthesis of pepsinogen was shown in isolated rabbit and human gastric glands after incubation of the glands in a 14C labelled amino acid enriched minimum Eagles medium. At regular intervals, glands and medium were separated and analysed by polyacrylamide gel electrophoresis. Newly synthesised pepsinogen was shown by autoradiography. Incorporation of 14C labelled amino acids was detected after only 30 min of culture and increased almost linearly in time for 4 h. By comparing the incorporation of label into total protein and into pepsinogen, it was concluded that pepsinogen formed 70-90% of the newly synthesised protein. Cimetidine, at a concentration of 160 micrograms/ml, strongly inhibited the synthesis of pepsinogen. Spontaneous secretion of pepsinogen into the medium was very low and relatively constant. Dibutyryl cyclic AMP considerably stimulated the secretion of pepsinogen into the medium. Histamine and pentagastrin did not influence the release of pepsinogen. These results show that isolated gastric glands are capable of synthesis and secretion of pepsinogen and that both can be selectively stimulated and inhibited.

Animals↗
PubMed1984

Effect of oral omeprazole on serum gastrin and serum pepsinogen I levels.

Fasting and meal-stimulated serum gastrin and serum pepsinogen I levels were determined in 8 healthy volunteers before, during, and after administration of 30 mg of omeprazole daily for 14 days. Fasting levels and the integrated increment of serum gastrin were significantly increased after 7 and 14 days of treatment with omeprazole, but not after a single dose. Fasting levels measured 2, 4, 7, 14, and 21 days after stopping treatment with omeprazole and the integrated increment of serum gastrin determined 7 and 14 days after discontinuation of omeprazole were not significantly different from pretreatment levels. Fasting serum pepsinogen I levels increased progressively during omeprazole treatment. This increase was significant after 7 and 14 days of treatment and 2 and 4 days after discontinuing omeprazole. These levels were not significantly different from pretreatment levels 7, 14, and 21 days after omeprazole treatment. Serum pepsinogen I did not significantly change after the test meal. It is concluded that fasting and meal-stimulated serum gastrin levels and fasting serum pepsinogen I levels increase significantly during treatment with 30 mg of omeprazole daily for 14 days, but after stopping treatment there is a rapid return to pretreatment levels.

Adult↗
PubMed1979

Genetic variation in parotid basic proteins (Pb) in the Bozo (Mali, West Africa).

The frequency of variants in the Pb system was studied in 71 individuals from the Bozo tribe in the Bani-Niger area (Mali, West Africa), in 25 male students from different African countries, and in 110 Dutch students. The frequency of the Pb2 allele was 0.20 in the Bozo and 0.00 in the Dutch population. A comparison is made with the results of a study among American blacks and with a Japanese study. The Pb 2--2 phenotypes observed in this study favour the hypothesis that the Pb-2 c protein is derived from a larger precursor in a manner analogous to the generation of the Pb-1 b protein from Pb-1 protein e.

Adolescent↗
PubMedDate not supplied

Relations between serum pepsinogen levels, pepsinogen phenotypes, ABO blood groups, age and sex in blood donors.

Serum pepsinogen A (pepsinogen I) levels and urinary pepsinogen A phenotypes were studied in relation to ABO blood group, age and sex in 700 healthy blood donors. There was no relation between urinary pepsinogen A phenotypes and serum pepsinogen A levels. It is concluded that serum PGA levels and PGA phenotypes are independent factors in predisposition to gastroduodenal disorders. Serum pepsinogen A levels were higher in males than in females and rose with increasing age. The ABO blood groups were not related to pepsinogen A phenotypes. Blood group O individuals showed higher serum pepsinogen A levels compared with blood group A. Pepsinogen A phenotypes with intensity of fraction 5 were more frequent in males compared with females.

ABO Blood-Group System↗