| 1. |
- Bengtsson, Magnus W., et al.
(författare)
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Duodenal bicarbonate secretion in rats : Stimulation by intra-arterial and luminal guanylin and uroguanylin
- 2007
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Ingår i: Acta Physiologica. - : Wiley. - 1748-1708 .- 1748-1716. ; 191:4, s. 309-317
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Uroguanylin and guanylin are endogenous ligands for guanylate cyclase C, an upstream regulator of the cystic fibrosis transmembrane resistance (CFTR) anion channel, and both peptides increase intestinal anion export in vitro. We have compared the effects of close intra-arterial and luminal administration of uroguanylin and guanylin on duodenal bicarbonate secretion in vivo and studied the interactions with melatonin and cholinergic stimulation. Methods: Lewis × Dark Agouti rats were anaesthetized and a segment of the proximal duodenum with intact blood supply was cannulated in situ. Mucosal bicarbonate secretion (pH stat) was continuously recorded and peptides were infused intra-arterially or added to the luminal perfusate. Results: Intra-arterial (50–1000 pmol kg−1 h−1) as well as luminal administration (50–500 nmol L−1) of guanylin or uroguanylin caused dose-dependent increases in the duodenal secretion. Luminal administration induced more rapidly appearing rises in secretion and the two peptides induced secretory responses of similar shape and magnitude. The melatonin MT2-selective antagonist luzindole (600 nmol kg−1) significantly depressed the response to intra-arterial guanylins but did not affect secretion induced by luminal guanylins. Similarly, the muscarinic antagonist atropine (0.75 μmol kg−1 followed by 0.15 μmol kg−1 h−1) abolished the response to intra-arterial uroguanylin but caused only slight suppression of the response to luminal uroguanylin. Conclusions: Intra-arterial as well as luminal uroguanylin and guanylin are potent stimuli of duodenal mucosal bicarbonate secretion in vivo. The response to luminal guanylins reflects an action at apical receptors. Stimulation by parenteral guanylins, in contrast, is under cholinergic influence and interacts with melatonin produced by mucosal enteroendocrine cells.
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| 2. |
- Bengtsson, Magnus W., et al.
(författare)
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Food-induced expression of orexin receptors in rat duodenal mucosa regulates the bicarbonate secretory response to orexin-A
- 2007
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Ingår i: American Journal of Physiology - Gastrointestinal and Liver Physiology. - : American Physiological Society. - 0193-1857 .- 1522-1547. ; 293:2, s. G501-G509
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Tidskriftsartikel (refereegranskat)abstract
- Presence of appetite-regulating peptides orexin-A and orexin-B in mucosal endocrine cells suggests a role in physiological control of the intestine. Our aim was to characterize orexin-induced stimulation of duodenal bicarbonate secretion and modulation of secretory responses and mucosal orexin receptors by overnight food deprivation. Lewis x Dark Agouti rats were anesthetized and proximal duodenum cannulated in situ. Mucosal bicarbonate secretion (pH stat) and mean arterial blood pressure were continuously recorded. Orexin-A was administered intra-arterially close to the duodenum, intraluminally, or into the brain ventricles. Total RNA was extracted from mucosal specimens, reverse transcribed to cDNA and expression of orexin receptors 1 and 2 (OX1 and OX2) measured by quantitative real-time PCR. OX1 protein was measured by Western blot. Intra-arterial orexin-A (60–600 nmol·h–1·kg–1) increased (P < 0.01) the duodenal secretion in fed but not in fasted animals. The OX1 receptor antagonist SB-334867, which was also found to have a partial agonist action, abolished the orexin-induced secretory response but did not affect secretion induced by the muscarinic agonist bethanechol. Atropine, in contrast, inhibited bethanechol but not orexin-induced secretion. Orexin-A infused into the brain ventricles (2–20 nmol·kg–1·h–1) or added to luminal perfusate (1.0–100 nM) did not affect secretion, indicating that orexin-A acts peripherally and at basolateral receptors. Overnight fasting decreased mucosal OX1 and OX2 mRNA expression (P < 0.01) as well as OX1 protein expression (P < 0.05). We conclude that stimulation of secretion by orexin-A may involve both receptor types and is independent of cholinergic pathways. Intestinal OX receptors and secretory responses are markedly related to food intake.
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| 3. |
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| 4. |
- Bengtsson, Magnus W., et al.
(författare)
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Short food deprivation inhibits orexin receptor 1 expression and orexin-A induced intracellular calcium signaling in acutely isolated duodenal enterocytes
- 2009
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Ingår i: American Journal of Physiology - Gastrointestinal and Liver Physiology. - : American Physiological Society. - 0193-1857 .- 1522-1547. ; 296:3, s. G651-G658
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Tidskriftsartikel (refereegranskat)abstract
- Bengtsson MW, Makela K, Herzig KH, Flemstrom G. Short food deprivation inhibits orexin receptor 1 expression and orexin-A induced intracellular calcium signaling in acutely isolated duodenal enterocytes. Am J Physiol Gastrointest Liver Physiol 296: G651-G658, 2009. First published December 31, 2008; doi:10.1152/ajpgi.90387.2008.-Close intra-arterial infusion of the appetite regulating peptide orexin-A stimulates bicarbonate secretion from the duodenal mucosa. The aim of the present study was to elucidate the ability of orexin-A to induce intracellular calcium signaling in acutely isolated duodenal enterocytes. Freshly isolated clusters of enterocytes, obtained from rat duodenal mucosa or human duodenal biopsies, were loaded with fura 2-AM and mounted in a perfusion chamber. Cryptlike enterocytes were selected (caged), and changes in intracellular calcium concentration ([Ca2+](i)) were evaluated by fluorescence imaging. Total RNA was extracted from pellets of enterocytes and reverse transcribed to cDNA, and expression of orexin receptors 1 and 2 (OX1R and OX2R) was measured by quantitative real-time PCR. Orexin-A at all concentrations tested (1-100 nM) increased [Ca2+](i) in enterocytes isolated from continuously fed rats, and the OX1R-antagonist SB-334867 (10 nM) attenuated the response. The primary [Ca2+](i) response was a slow increase to a sustained plateau persisting after orexin-A removal, and a similar response was observed in enterocytes from human biopsies. In contrast to orexin-A, the OX2R agonist (Ala(11), D-Leu(15))orexin-B (1-10 nM) did not induce calcium signaling. There were no significant [Ca2+](i) responses in enterocytes from animals food deprived overnight, and overnight fasting decreased (P < 0.01) enterocyte OX1R as well as OX2R mRNA. Induction of intracellular calcium signaling in isolated duodenal enterocytes is thus mediated primarily by OX1R receptors. Short (overnight) food deprivation markedly depresses receptor expression and inhibits orexin-A induced increases in [Ca2+](i). Studies of enterocyte signaling and intestinal secretion requires particular evaluation regarding feeding status.
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| 5. |
- Cinthio, Magnus, et al.
(författare)
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It is possible to resolve micrometer movements in B-mode images
- 2012
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Ingår i: 2012 IEEE International Ultrasonics Symposium (IUS). ; , s. 2536-2539
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Konferensbidrag (refereegranskat)abstract
- We have proposed an echo localization estimator which theoretically gives infinite resolution in the axial direction in ultrasonic B-mode images during 1) echo structure tracking and 2) distance measurements of distinct echoes. The performance of the estimator was evaluated using a HDI5000 (Philips Medical Systems, Bothell, WA, USA) with a 35 mm 5-12 MHz linear array transducer. The resulting pixel size in the B-mode image was 100 mu m. The controlled setup consisted of a small water container lined with ultrasound absorber carpet and placed on a micrometer table, a triangulation laser (M5L/2, MEL Mikroelektronik GmbH, Eching, Germany) connected to a high-performance digital multimeter HP 34401A (Agilent Technologies, USA) and a thermometer TESTO 925 (Testo AG, Germany). In each of the three measurement series the micrometer table was moved approximately 15 mu m in 10-12 steps. The echo localization estimator succeeded to resolve the minute movement (< 20 mu m) with high agreement with the reference method in all three series. The correlation was (R>0.998; p <10-e38; 0.86
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| 6. |
- Esmaily, Mohsen, 1987, et al.
(författare)
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Atmospheric Corrosion of Mg Alloy AZ91D Fabricated by aSemi-Solid Casting Technique: The Influence of Microstructure
- 2015
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Ingår i: Journal of the Electrochemical Society. - : The Electrochemical Society. - 0013-4651 .- 1945-7111. ; 162:7, s. C311-C321
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Tidskriftsartikel (refereegranskat)abstract
- The atmospheric corrosion behavior of alloy AZ91D produced by a semi-solid metal (SSM) technique and by conventional high pressure die casting (HPDC) was investigated for up to 1176 hours in the laboratory. Alloy AZ91D in the SSM state was fabricated using a rheocasting (RC) technique in which the slurry was prepared by the RheoMetal process. Exposures were performed in 95% RH air at 22 and 4 degrees C. The RC alloy AZ91D exhibited significantly better corrosion resistance than the HPDC material at two temperatures studied. The effect of casting technology on corrosion is explained in terms of the microstructural differences between the materials. For example, the larger number density of cathodic beta phase particles in the HPDC material initially causes relatively rapid corrosion compared to the RC material. During later stages of corrosion, the more network-like beta phase particles in the RC alloy act as a corrosion barrier, further improving the relative corrosion resistance of the RC material.
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| 7. |
- Sjöblom, Markus, et al.
(författare)
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Cholecystokinin but not ghrelin stimulates mucosal bicarbonate secretion in rat duodenum : Independence of feeding status and cholinergic stimuli
- 2013
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Ingår i: Regulatory Peptides. - : Elsevier BV. - 0167-0115 .- 1873-1686. ; 183, s. 46-53
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Tidskriftsartikel (refereegranskat)abstract
- Cholecystokinin (CCK) is an important regulator of food digestion but its influence on small intestinal secretion has received little attention. We characterized effects of CCK-8, ghrelin and some related peptides on duodenal HCO3- secretion in vivo and demonstrated CCK-induced calcium signaling in acutely isolated enterocytes. A segment of proximal duodenum with intact blood supply was cannulated in situ in anaesthetized rats. Mucosal HCO3- secretion was continuously recorded (pH-stat). Peptides were administrated to the duodenum by close intra-arterial infusion. Clusters of duodenal enterocytes were attached to the bottom of a perfusion chamber. The intracellular calcium concentration ([Ca2+](i)) was examined by dual-wavelength imaging. CCK-8 (3.0, 15 and 60 pmol/kg,h) caused dose-dependent increases (p < 0.01) in duodenal alkaline secretion in both overnight fasted and continuously fed animals. The CCK1R-antagonist devazepide but neither the CCK2R-antagonist YMM022 nor the melatonin MT2-selective antagonist luzindole inhibited the rise in secretion. Atropine decreased sensitivity to CCK-8. The appetite-related peptide ghrelin was without effect on the duodenal secretion in fasted as well as fed animals. Superfusion with CCK-8 (1.0-50 nM) induced [Ca2+](i) signaling in acutely isolated duodenal enterocytes. After an initial peak response, [Ca2+](i) returned to near basal values within 3-5 min. Devazepide but not YMM022 inhibited this [Ca2+](i) response. Low doses of CCK-8 stimulate duodenal alkaline secretion and induce enterocyte [Ca2+](i) signaling by an action at CCK1 receptors. The results point to importance of CCK in the rapid postprandial rise in mucosa-protective duodenal secretion.
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