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  • bombesin  (2)
  • pancreatic cancer  (2)
  • rats  (2)
  • 1
    ISSN: 1573-2568
    Keywords: aging ; gastric secretion ; gastrin ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The purpose of this study was to characterize the effects of aging on gastric acid secretion and on serum and antral concentrations of gastrin in rats. Young and old Fischer 344 rats were prepared with gastric fistulas. Twenty-four hours after surgery, graded doses of human synthetic gastrin-17 (SHG-17) (2, 5, 10, 20, and 40 μg/kg) were given intravenously in random order. Gastric secretions were collected for gastric acid measurement before and at 15-min intervals after each dose of gastrin. In a separate study, blood was collected and the stomachs were removed for antral gastrin extraction from fed young and old rats. Serum and antral gastrin was measured by radioimmunoassay. The basal and gastrin-stimulated acid secretions were significantly decreased in aged rats compared to the young rats. The basal acid output was 0.4±0.2 μeq/15 min in the aged rats and 1.5±0.5 μeq/15 min in the young. The maximal acid output stimulated by gastrin was 11.1±1.8 μeq/15 min in the aged rats and 24.2±2.8 μeq/15 min in the young. Both serum and antral concentrations of gastrin were significantly decreased in aged rats. Serum gastrin concentration was 114.8±7.4 pg/ml in the aged rats and 192.0±14.4 pg/ml in the young. Antral gastrin concentration was 3.9±0.5 μg/g tissue in the aged rats, which was significantly less than the concentration in the young (6.5±0.4 μg/g tissue). Antral gastrin content did not change with aging. Gastric acid secretion in aged rats is significantly decreased compared to the young in both the basal condition and in response to fixed doses of exogenous gastrin. Diminished concentrations of circulating gastrin may well be responsible, at least in part, for the diminished acid secretion in the aged rats.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-0646
    Keywords: polyamines ; pancreatic cancer ; colon cancer ; cyclosporine ; DFMO
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have previously reported that the in vitro growth of MC-26 mouse colon cancer and H2T hamster pancreatic cancer cells are inhibited by cyclosporine (CsA) and α-difluoromethylornithine (DFMO). The present study was designed to investigate the effects of these two drugs on the two experimental tumors (MC-26 and H2T) growing in vivo. Forty-eight male Balb/c mice or Syrian golden hamsters were inoculated with MC-26 (250,000) or H2T (500,000) cells, respectively, and then were randomized into four groups of 12 each: group I was control; group II received CsA; group III received DFMO; group IV received a combination of CsA and DFMO. MC-26 tumors were significantly more sensitive than H2T tumors to the effects of CsA and DFMO. MC-26 tumor growth and tumor weight, as well as the tumor content of DNA, RNA, and protein were all significantly more reduced by CsA and DFMO than were the H2T tumors. Our present study shows that both CsA and DFMO are potent inhibitors of MC-26 colon carcinoma growth in vivo, though DFMO is more than twice as effective as CsA. DFMO also produced greater reductions in the tumor content of DNA, RNA, and protein than did CsA. DFMO significantly decreased the concentrations of polyamines in both H2T and MC-26 tumors; the MC-26 tumors were affected to a greater degree.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: okadaic acid ; retinoblastoma protein ; pancreatic cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Phosphorylation/dephosphorylation of intracellular proteins are important steps in the regulation of cell growth. Okadaic acid, an inhibitor of the serine/threonine protein phosphatases 1 and 2A, is a potent tumor promoter. This effect may be through the inhibition of dephosphorylation (termed “hyperphosphorylation”) and subsequent inactivation of tumor-suppressor proteins. We examined whether okadaic acid regulates growth of human pancreatic cancer cells (MIA PaCa-2 and Panc-1) or alters the phosphorylation of the retinoblastoma tumor-suppressor protein. Growth studies, nuclear labeling analyses, and Western blotting for retinoblastoma protein were performed. Okadaic acid stimulated cell growth and induced hyperphosphorylation of the retinoblastoma protein. The growth-stimulatory effect of okadaic acid on these human pancreatic cancer cells may be mediated by inactivation of the growth suppressive effect of the retinoblastoma protein by hyperphosphorylation. These studies suggest that the growth of these human pancreatic cancer cells is still regulated by tumor-suppressor proteins.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: gastrinoma ; bombesin ; growth ; gastrin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The growth of the human gastrinoma model (PT) in athymic nude mice is stimulated by bombesin (BBS), an amphibian peptide homologous to both human gastrin-releasing peptide (GRP) and neuromedin B (NMB). The mechanism is not known, and a potent and specific GRP-R antagonist BIM26226, which has low affinity for NMB-R, was usedin vivo in athymic nude mice bearing gastrinoma subcutaneously. Both the BBS and BIM26226 stimulated the growth of PT, and the growth stimulation was even greater when given together. RT-PCR study of gastrinoma revealed the presence of both GRP-R and NMB-R mRNA, but much more abundant NMB-R mRNA. We conclude that BBS-stimulated growth of gastrinoma involves both GRP-R and NMB-R, and our findings suggest that GRP-R mediates negative and NMB-R produces positive growth effects on gastrinoma.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: burns ; starvation ; gut ; apoptosis ; proliferation ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Maintenance of gut mucosal homeostasis depends on a balance between cell proliferation and cell death. Gut mucosal integrity is impaired after severe burn and during starvation. We determined the effect of burn, starvation, and the combination of both on small bowel epithelial apoptosis and proliferation. Fifty adult male Fischer 344 rats (260–300 g) received a 60% full-thickness scald burn and were randomly divided into fed and starved groups. Small intestine was taken at 12, 24, and 48 hr after injury. All animals in the 12-hr group were starved while recovering from anesthesia. Apoptosis was quantified by immunohistochemical staining (TUNEL) and mucosal proliferation was determined by bromodeoxyuridine (BrdU) incorporation. The apoptotic index was higher in burned rats compared to controls at 12 hr after burn; both these groups were starved (P 〈 0.05). At 24 and 48 hr after burn, apoptosis was highest in the starved groups, with no additional effects of burn (P 〈 0.05). Mucosal epithelial cell proliferation was not different between groups at any time point. In conclusion, burn and starvation both increase apoptosis in the small bowel mucosa; however, these effects are not additive. Apoptosis could be attenuated by enteral feeding, which delineates the importance of early enteral feeding initiation after injury to maintain mucosal integrity.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-2568
    Keywords: bombesin ; carbachol ; peptone ; Fischer 344 rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have examined the release of gastrin and somatostatin from the isolated perfused stomach of rats of three different age groups (4 months, 12 months, and 24 months old) in response to bombesin and carbachol. The basal release of gastrin was diminished in 24-month-old rats. Basal somatostatin release showed an age-related decrease. Bombesin (10−10 and 10−9 M) and carbachol (10−8 and 10−7 M) stimulated gastrin release in each age group. The integrated release of gastrin in response to bombesin (10−10 and 10−9 M) or carbachol (10−8 M) did not differ among the three age groups, although integrated gastrin release in response to carbachol (10−7 M) decreased in 24-month-old rats. Bombesin-stimulated release of somatostatin decreased in 12- and 24-month-old rats. Carbachol inhibited release of somatostatin in each age group. Compared with 4-month-old rats, the inhibition of somatostatin release by carbachol was less in 24-month-old rats at 10−8 and 10−7 M, and less in 12-month-old rats at 10−7 M. The decreased basal gastrin secretion and well-preserved gastrin response were further confirmed in conscious aged rats tested by means of oral gavage with 10% peptone. Our findings indicate that gastrin response to the stimuli is well preserved with aging, whereas the response of somatostatin diminishes in an age-related manner. Aging has different effects on the release of gastrin and somatostatin from the rat stomach.
    Type of Medium: Electronic Resource
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