| 1. |
- Björkqvist, Maria, et al.
(författare)
-
Somatostatin, misoprostol and galanin inhibit gastrin- and PACAP-stimulated secretion of histamine and pancreastatin from ECL cells by blocking specific Ca(2+) channels.
- 2005
-
Ingår i: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 130:1-2, s. 81-90
-
Tidskriftsartikel (refereegranskat)abstract
- The oxyntic mucosa is rich in ECL cells. They secrete histamine and chromogranin A-derived peptides, such as pancreastatin, in response to gastrin and pituitary adenylate cyclase-activating peptide (PACAP). Secretion is initiated by Ca2+ entry. While gastrin stimulates secretion by opening L-type and N-type Ca2+ channels, PACAP stimulates secretion by activating L-type and receptor-operated Ca2+ channels. Somatostatin, galanin and prostaglandin E2 (PGE2) inhibit gastrin- and PACAP-stimulated secretion from the ECL cells. In the present study, somatostatin and the PGE2 congener misoprostol inhibited gastrin- and PACAP-stimulated secretion 100%, while galanin inhibited at most 60–65%. Bay K 8644, a specific activator of L-type Ca2+ channels, stimulated ECL-cell secretion, an effect that was inhibited equally effectively by somatostatin, misoprostol and galanin (75–80% inhibition). Pretreatment with pertussis toxin, that inactivates inhibitory G-proteins, prevented all three agents from inhibiting stimulated secretion (regardless of the stimulus). Pretreatment with nifedipine (10 μM), an L-type Ca2+ channel blocker, reduced PACAP-evoked pancreastatin secretion by 50–60%, gastrin-evoked secretion by not, vert, similar 80% and abolished the response to Bay K 8644. The nifedipine-resistant response to PACAP was abolished by somatostatin and misoprostol but not by galanin. Gastrin and PACAP raised the intracellular Ca2+ concentration in a biphasic manner, believed to reflect mobilization of internal Ca2+ followed by Ca2+ entry. Somatostatin and misoprostol blocked Ca2+ entry (and histamine and pancreastatin secretion) but not mobilization of internal Ca2+. The present observations on isolated ECL cells suggest that Ca2+ entry rather than mobilization of internal Ca2+ triggers exocytosis, that gastrin and PACAP activate different (but over-lapping) Ca2+ channels, that somatostatin, misoprostol and galanin interact with inhibitory G-proteins to block Ca2+ entry via L-type Ca2+ channels, and that somatostatin and misoprostol (but not galanin) in addition block N-type and/or receptor-operated Ca2+ channels.
|
|
| 2. |
- Florentzson, Malin, et al.
(författare)
-
Low gastric acid and high plasma gastrin in high-anxiety Wistar Kyoto rats
- 2009
-
Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 44:4, s. 401-407
-
Tidskriftsartikel (refereegranskat)abstract
- Objective. Wistar Kyoto (WKY) rats are more susceptible to stress-evoked ulcerations than Sprague-Dawley (SPD) rats. We have already demonstrated that gastrin cells are more active and ghrelin cells less active in WKY rats than in SPD rats. The purpose of this study was to compare endocrine cell activity and gastric acid output in WKY and SPD rats. Material and methods. Gastric acid output was determined in conscious rats with gastric fistula. Plasma gastrin and ghrelin levels were measured after an overnight fast. Acid secretagogues (gastrin, histamine and carbachol) were given by continuous subcutaneous infusion. Results. The volume of gastric juice, and the acidity and acid output were all significantly lower (p 0.05) in fasted WKY rats than in fasted SPD rats. Gastrin evoked a 4-fold (p 0.01) and 3-fold (p 0.05) increase in gastric acid output in SPD rats and WKY rats, respectively. Histamine raised the acid output 1.6-fold in SPD rats (p=0.06) and 3-fold in WKY rats (p 0.05), while carbachol failed to affect the acid output (weak increase, p 0.05). Fasting plasma ghrelin levels were 2-fold higher in SPD rats than in WKY rats (p 0.01) while fasting gastrin levels were 10-fold higher in WKY rats than in SPD rats (p 0.05). Neither the parietal-cell density nor the oxyntic mucosal thickness differed between the two strains. Conclusions. The results of the present study suggest that a high gastrin cell activity in WKY rats is secondary to a low gastric acidity. Whether the high gastrin cell activity is linked to susceptibility to stress ulcer in WKY rats warrants further investigation.
|
|
| 3. |
|
|
| 4. |
- Persson, Jonas, et al.
(författare)
-
Strain effects on individual quantum dots: Dependence of cap layer thickness
- 2005
-
Ingår i: Physical Review B (Condensed Matter and Materials Physics). - 1098-0121. ; 72:8
-
Tidskriftsartikel (refereegranskat)abstract
- We have studied the effects of strain on individual self-assembled quantum dots (QDs) exemplified by InP dots embedded in GaInP. The quantum dot sample was etched from the top and in this way the amount of capping material was reduced. In a sequence of etch cycles, the cap layer was thinned, and the photoluminescence from several individual QDs could be followed as a function of cap layer thickness. The evolution of the emission spectra clearly depended on the quantum dot size. We interpret this as arising from differences in the aspect ratio for quantum dots of different sizes. The influence of the capping layer, for different QD geometries, was modeled using deformation potential theory with the strain calculated using a full three-dimensional linear elasticity model. The results agree well with the experimental observations.
|
|
| 5. |
- Sand, Elin, et al.
(författare)
-
High gastrin cell activity and low ghrelin cell activity in high-anxiety Wistar Kyoto rats
- 2007
-
Ingår i: Journal of Endocrinology. - 1479-6805. ; 193:2, s. 245-250
-
Tidskriftsartikel (refereegranskat)abstract
- Ghrelin is produced by gastric A-like cells and released in response to food deprivation. Interestingly, psychological stress also raises circulating ghrelin levels. This study compared plasma ghrelin levels in Sprague-Dawley (SPD) rats and high-anxiety Wistar Kyoto (WKY) rats. The two strains were also compared with respect to plasma gastrin, a gastric hormone with a pre- and postprandial release pattern opposite to that of ghrelin, and to the activity of the gastrin-dependent, histamine-forming ECL cells in the gastric mucosa. The rats were killed after being freely fed or after an over-night fast. The stomachs were weighed and tissue samples were collected for histological and biochemical analysis. Plasma ghrelin and gastrin levels were determined by RIA. While fasted SPD rats had higher plasma ghrelin levels than fasted WKY rats (P<0 center dot 001), plasma ghrelin did not differ between freely fed rats of the two strains. Gastrin levels were higher in fed WKY rats than in fed SPD rats (P< 0 center dot 001). Despite the higher plasma gastrin level, the oxyntic mucosal histidine decarboxylase (HDC) activity (a marker of ECL-cell activity) in fed rats and the mucosal thickness did not differ between the two strains. In a subsequent study, rats were subjected to water-avoidance stress for 60 min, causing plasma gastrin to increase in WKY rats (P<0 center dot 001) but not in SPD rats. In conclusion, high-anxiety WKY rats had lower circulating ghrelin and higher gastrin than SPD rats in both the fasted and fed state, while the ECL-cell activity (HDC activity) was only moderately affected.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
- Vanky, Farkas B, et al.
(författare)
-
Long-Term Consequences of Postoperative Heart Failure After Surgery for Aortic Stenosis Compared With Coronary Surgery
- 2007
-
Ingår i: Annals of Thoracic Surgery. - : Elsevier BV. - 0003-4975 .- 1552-6259. ; 83:6, s. 2036-2043
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Although postoperative heart failure is a major determinant of operative mortality in cardiac surgery it has received little attention in the literature, and long-term consequences remain to be addressed. Therefore, the impact of postoperative heart failure on long-term survival in relation to other risk factors was studied. Methods: All patients undergoing aortic valve replacement (AVR) for aortic stenosis from 1995 through 2000 in the southeast region of Sweden (n = 398) were compared with a cohort, matched for age and sex, undergoing coronary artery bypass grafting (CABG [n = 398]). Risk factors for 5-year mortality were analyzed. Results: Forty-five AVR and 47 CABG patients required treatment for postoperative heart failure. Thirty-day, 1-year, and 5-year mortality in patients with and without postoperative heart failure after AVR were 6.7% versus 1.4% (p = 0.05), 8.9% versus 4.0% (p = 0.13), and 42.2% versus 14.2% (p < 0.0001) respectively. Corresponding results in the CABG group were 21.3% versus 1.1% (p < 0.0001), 25.5% versus 3.1% (p < 0.0001), and 36.2% versus 11.1% (p = 0.0015). Postoperative heart failure, preoperative renal dysfunction, procedure-associated stroke, body mass index less than 19 kg/m2, older age, preoperative atrial fibrillation, and preoperative anemia turned out as independent risk factors for 5-year mortality after AVR. In the CABG group, postoperative heart failure, diabetes mellitus, older age, and procedure-associated stroke emerged as independent risk factor for 5-year mortality. Conclusions: Postoperative heart failure was associated with high early mortality after CABG whereas the grave consequences of postoperative heart failure after AVR for aortic stenosis became evident only with time. © 2007 The Society of Thoracic Surgeons.
|
|
