Готові списки джерел за темами / Glandes submucosales

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Добірка наукової літератури з теми "Glandes submucosales"

Автор: Grafiati

Опубліковано: 14 грудня 2024

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Статті в журналах з теми "Glandes submucosales"

Melgarejo-Moreno, Pablo, and Diego Hellin-Meseguer. "Different glycoconjugates in the submucosal glands of the supraglottis and subglottis. Lectin histochemistry study in the hamster." Journal of Laryngology & Otology 111, no. 5 (May 1997): 441–43. http://dx.doi.org/10.1017/s0022215100137582.

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AbstractA lectin histochemistry study was performed in the supraglottic and subglottic regions of 10 hamsters. The submucosal glands were observed by light microscopy. The supraglottic submucosal glands presented numerous mucous tubules but on the other hand, the subglottic submucosal glands had serous tubules which finished at the distal portion in serous acini. The results suggest that the distribution of fucosylatedmucin and serum-type glycloproteins between the supra- and subglottic submucosal glands suggest a different viscosity and function of the mucus.

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Hopwood, D., G. Coghill, and D. S. A. Sanders. "Human oesophageal submucosal glands." Histochemistry 86, no. 1 (1986): 107–12. http://dx.doi.org/10.1007/bf00492353.

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Somogyvári, Krisztina, Péter Móricz, Imre Gerlinger, László Kereskai, István Szanyi, and Ildikó Takács. "Morphological and Histological Effects of Radiofrequency and Laser (KTP and Nd:YAG) Treatment of the Inferior Turbinates in Animals." Surgical Innovation 24, no. 1 (October 13, 2016): 5–14. http://dx.doi.org/10.1177/1553350616673452.

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The aim of this study was to evaluate the short and medium-term effects of radiofrequency (RF) and potassium titanyl phosphate (KTP) and neodymium-yttrium-aluminum garnet (Nd:YAG) laser treatment on the inferior turbinate mucosa in a porcine model. Following randomization, the inferior turbinates were treated either with RF submucosally or with the KTP or the Nd:YAG laser on the surface under videoendoscopic control. Tissue samples were taken at the end of postoperative weeks 1 and 6, and were evaluated macroscopically and histopathologically. Scanning electron microscopy was implemented to demonstrate the morphological changes in the respiratory epithelium. Six weeks following the RF procedure, the mucosa was intact in all cases, and the volume of the inferior turbinates was reduced in the majority of the cases. Although a volume reduction occurred in both laser groups, more complications associated with the healing procedure were noted. With hematoxylin and eosin and periodic acid–Schiff staining, intact epithelium, and submucosal glands remained after the RF procedures at the end of postoperative week 6. Following the KTP-laser intervention, necrotizing sialometaplasia and cartilage destruction occurred, and squamous metaplasia was also apparent in the Nd:YAG group. In both laser groups, dilated glands with excess mucus were seen. The scanning electron microscopic findings demonstrated that cilia were present in all cases. In conclusion, the medium-term macroscopic results were similar in all 3 groups, but the postoperative complications were less following the RF procedure. RF procedure is minimally invasive due to the submucosal intervention that leads to a painless, function preserving recovery.

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Moore, Beverley A., David Kim, and Stephen Vanner. "Neural pathways regulating Brunner's gland secretion in guinea pig duodenum in vitro." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 5 (November 1, 2000): G910—G917. http://dx.doi.org/10.1152/ajpgi.2000.279.5.g910.

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This study examined the neural pathways innervating Brunner's glands using a novel in vitro model of acinar secretion from Brunner's glands in submucosal preparations from the guinea pig duodenum. Neural pathways were activated by focal electrical stimulation and excitatory agonists, and videomicroscopy was used to monitor dilation of acinar lumen. Electrical stimulation of perivascular nerves evoked large dilations that were blocked by TTX (1 μM) or the muscarinic receptor antagonist 4-diphenylacetoxy- N-(2-chloroethyl)-piperidine hydrochloride (1 μM). The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (100 μM) had no effect, and the nerve-evoked responses were not inhibited by hexamethonium (200 μM). Dilations were abolished in preparations from chronically vagotomized animals. Activation of submucosal ganglia significantly dilated submucosal arterioles but not Brunner's glands. Effects of electrical stimulation of perivascular and submucosal nerves were not altered by guanethidine. Capsaicin and substance P also dilated arterioles but had no effect on Brunner's glands. Cholinergic (choline acetyltransferase-immunoreactive) nerve fibers were found in Brunner's glands. These findings demonstrate that Brunner's glands are innervated by cholinergic vagal fibers but not by capsaicin-sensitive or intrinsic enteric nerves.

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Sasaki, T., S. Shimura, H. Sasaki, and T. Takishima. "Effect of epithelium on mucus secretion from feline tracheal submucosal glands." Journal of Applied Physiology 66, no. 2 (February 1, 1989): 764–70. http://dx.doi.org/10.1152/jappl.1989.66.2.764.

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We studied the effect of airway epithelium on mucus secretion by use of an isolated tracheal submucosal gland preparation reported previously (J. Appl. Physiol. 60: 1237–1247, 1986). Mucus glycoconjugate release from submucosal glands of feline trachea was examined using [3H]glucosamine as a mucus precursor. Isolated glands showed significantly higher secretory responses to cholinergic, alpha-, and beta-adrenergic agonists and dibutyryladenosine 3′,5′-cyclic monophosphate (average 400% of control) than the conventional tracheal mucosal explants, which contained epithelium and submucosal tissues in addition to submucosal glands (average 160% of control). The addition of isolated epithelium depressed the secretory response of isolated glands to the same level as that of tracheal explants. However, the supernatant from isolated epithelium failed to inhibit secretory responses to methacholine in isolated glands, suggesting that the epithelium-derived inhibitory factor to secretion may be short-lived. Leukotriene D4 antagonist (FPL 55712), cyclooxygenase and/or lipoxygenase inhibitors (indomethacin or BW 755C) caused no significant change in the inhibitory action of epithelium, suggesting that the inhibition is not due to arachidonic acid metabolites. The newly found secretory inhibitory action of epithelium is of particular interest in the pathogenesis of hypersecretion associated with epithelial damage.

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Pilewski, J. M., J. F. Engelhardt, J. E. Bavaria, L. R. Kaiser, J. M. Wilson, and S. M. Albelda. "Adenovirus-mediated gene transfer to human bronchial submucosal glands using xenografts." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 4 (April 1, 1995): L657—L665. http://dx.doi.org/10.1152/ajplung.1995.268.4.l657.

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The cystic fibrosis (CF) transmembrane conductance regulator has been localized to both submucosal glands and surface epithelium, suggesting that both glandular and surface epithelium may be important targets for gene therapy. To determine the distribution and efficiency of recombinant adenovirus-mediated gene transfer to human airway submucosal glands, an in vivo model was developed by heterotopically transplanting human bronchial segments from both normal and CF lung tissue into severe combined immunodeficient mice. A serotype 5 E1-deleted recombinant adenovirus containing a lacZ reporter gene driven by the cytomegalovirus promoter (H5.010CMVlacZ) was used to infect the xenografts. Transgene expression was correlated with three factors: 1) viral titer, 2) penetration of microspheres, and 3) dwell time of the viral instillate. At viral titers ranging from 10(8) to 10(11) plaque forming units/ml, expression of the lacZ gene was observed in a subpopulation of epithelial cells within approximately 40% of submucosal glands, with more efficient gene transfer to the ducts than the secretory tubules. Within individual glands, gene transfer varied from < 1% to approximately 20% of submucosal cells, including duct, mucous, and serous cells. Adenovirus-sized fluorescent microspheres were found to penetrate only some of the submucosal glands, suggesting that the gene transfer efficiency to submucosal tubules is due to limited viral particle penetration rather than tropism. Gene transfer to surface epithelial cells was inefficient. However, the percentage of transduced surface epithelial cells increased from < 1% to 5–10% as the dwell time of viral solution was increased from 5 min to 1 h, indicating that the time allowed for virus binding and entry is important for gene transfer efficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

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Wine, J. J. "Submucosal Glands and Airway Defense." Proceedings of the American Thoracic Society 1, no. 1 (January 1, 2004): 47–53. http://dx.doi.org/10.1513/pats.2306015.

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Baniak, Nicholas, Xiaojie Luan, Amber Grunow, Terry E. Machen та Juan P. Ianowski. "The cytokines interleukin-1β and tumor necrosis factor-α stimulate CFTR-mediated fluid secretion by swine airway submucosal glands". American Journal of Physiology-Lung Cellular and Molecular Physiology 303, № 4 (15 серпня 2012): L327—L333. http://dx.doi.org/10.1152/ajplung.00058.2012.

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The airway is kept sterile by an efficient innate defense mechanism. The cornerstone of airway defense is mucus containing diverse antimicrobial factors that kill or inactivate pathogens. Most of the mucus in the upper airways is secreted by airway submucosal glands. In patients with cystic fibrosis (CF), airway defense fails and the lungs are colonized by bacteria, usually Pseudomonas aeruginosa . Accumulating evidence suggests that airway submucosal glands contribute to CF pathogenesis by failing to respond appropriately to inhalation of bacteria. However, the regulation of submucosal glands by the innate immune system remains poorly understood. We studied the response of submucosal glands to the proinflammatory cytokines interleukin-1β and tumor necrosis factor-α. These are released into the airway submucosa in response to infection with the bacterium P. aeruginosa and are elevated in CF airways. Stimulation with IL-1β and TNF-α increased submucosal gland secretion in a concentration-dependent manner with a maximal secretion rate of 240 ± 20 and 190 ± 40 pl/min, respectively. The half maximal effective concentrations were 11 and 20 ng/ml, respectively. The cytokine effect was dependent on cAMP but was independent of cGMP, nitric oxide, Ca2+, or p38 MAP kinase. Most importantly, IL-1β- and TNF-α-stimulated secretion was blocked by the CF transmembrane conductance regulator (CFTR) blocker, CFTRinh172 (100 μmol/l) but was not affected by the Ca2+-activated Cl− channel blocker, niflumic acid (1 μmol/l). The data suggest, that during bacterial infections and resulting release of proinflammatory cytokines, the glands are stimulated to secrete fluid, and this response is mediated by cAMP-activated CFTR, a process that would fail in patients with CF.

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Eguchi, Koichi, Kunihiko Aoyagi, Satoshi Nimura, and Shotaro Sakisaka. "Diagnostic Value of Endoscopic and Endoscopic Ultrasound Characteristics of Duodenal Submucosal Tumour-Like Heterotopic Gastric Mucosa." Canadian Journal of Gastroenterology 25, no. 7 (2011): 365–67. http://dx.doi.org/10.1155/2011/104815.

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OBJECTIVE: Recent studies have reported that duodenal heterotopic gastric mucosa (HGM) has been observed in 8.9% of patients who undergo esophagogastroduodenoscopy. However, there are few reports concerning the endoscopic and endoscopic ultrasound characteristics of submucosal tumour-like HGM in the duodenum.METHODS: Endoscopic, endoscopic ultrasound (EUS) and histological findings were analyzed in six patients with submucosal tumour-like HGM, which were confirmed by pathological examination of biopsy or endoscopic polypectomy specimens.RESULTS: Endoscopically, the lesions appeared as a solitary, sessile submucosal tumour-like mass with a depression at the top. In four of six patients, small granular structures were found in the depressed area of the mass. On EUS, all masses demonstrated a heterogeneous pattern, among which four patients presented anechoic areas while two patients showed no anechoic areas. All lesions were localized within the mucosa and submucosa on EUS. Histologically, they consisted of gastric glands and some dilated glands, and were covered with normal duodenal epithelium. In four of six lesions, the tumours were composed of gastric-type foveolar epithelium showing papillary growth, fundic glands and pyloric glands, while the others consisted of gastric-type foveolar epithelium and pyloric glands.CONCLUSION: A heterogeneous pattern on EUS and small granular structures on esophagogastroduodenoscopy represent valuable diagnostic features of submucosal tumour-like HGM.

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Duan, D., Y. Yue, W. Zhou, B. Labed, T. C. Ritchie, R. Grosschedl, and J. F. Engelhardt. "Submucosal gland development in the airway is controlled by lymphoid enhancer binding factor 1 (LEF1)." Development 126, no. 20 (October 15, 1999): 4441–53. http://dx.doi.org/10.1242/dev.126.20.4441.

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Previous studies have demonstrated that transcription of the lymphoid enhancer binding factor 1 (Lef1) gene is upregulated in submucosal gland progenitor cells just prior to gland bud formation in the developing ferret trachea. In the current report, several animal models were utilized to functionally investigate the role of LEF1 in initiating and supporting gland development in the airway. Studies on Lef1-deficient mice and antisense oligonucleotides in a ferret xenograft model demonstrate that LEF1 is functionally required for submucosal gland formation in the nasal and tracheal mucosa. To determine whether LEF1 expression was sufficient for the induction of airway submucosal glands, two additional model systems were utilized. In the first, recombinant adeno-associated virus was used to overexpress the human LEF1 gene in a human bronchial xenograft model of regenerative gland development in the adult airway. In a second model, the LEF1 gene was ectopically overexpressed under the direction of the proximal airway-specific CC10 promoter in transgenic mice. In both of these models, morphometric analyses revealed no increase in the number or size of airway submucosal glands, indicating that ectopic LEF1 expression alone is insufficient to induce submucosal gland development. In summary, these studies demonstrate that LEF1 expression is required, but in and of itself is insufficient, for the initiation and continued morphogenesis of submucosal glands in the airway.

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Більше джерел

Дисертації з теми "Glandes submucosales"

Meziane, Chabane. "Modélisation mathématique et simulation numérique du transport mucociliaire." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASM042.

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Le transport de fluide biologique par le mouvement des cils est un phénomène naturel qu’on retrouve chez presque tous les êtres vivants. Le but de cette thèse est la modélisation et la simulation numérique de la clairance mucociliaire, faisant intervenir l’action des cils sur le fluide visqueux (composé de mucus et du liquide périciliaire), modélisé par des équations de Stokes. Le modèle fait intervenir aussi la sécrétion du mucus par les cellules sécrétrices, présentes au niveau de l’épithélium bronchique. Le premier chapitre traite de la modélisation 3D de l’écoulement du fluide sous l’action des cils, dont la contribution est modélisée par une courbe 1D représentant la ligne centrale du cil. Le problème résultant est un problème de Stokes singulier et non-local. Dans le chapitre 2 nous avons étudié, dans un modèle d’arbre bronchique symétrique dyadique, les épaisseurs de la couche mucus à l’équilibre, résultant de la sécrétion du mucus par l’épithélium, et de l’évacuation du mucus par les cils d’autre part. Enfin dans le chapitre 3, nous avons étudié l’influence de l’écoulement d’air à travers la lumière bronchique sur l’efficacité de la clairance mucociliaire, et ce, dans un régime de respiration normale, fort, puis extrême
The transport of biological fluid by the movement of cilia is a natural phenomenon found in almost all living beings. The aim of this thesis is the modeling and numerical simulation of mucociliary clearance, involving the action of cilia on the viscous fluid (composed of mucus and PCL), modeled by Stokes equations. As well as the secretion of mucus by the submucosal glands and the goblet cells, present in the bronchial epithelium. The first chapter deals with the 3D modeling of the fluid flow under the action of the cilia, the contribution of which is modeled by a 1D curve representing the central line of the cilium. The resulting problem is a singular and non-local Stokes problem. In Chapter 2, we studied in a model of a symmetrical dyadic bronchial tree, the thickness of the mucus layer at equilibrium, resulting from the secretion of mucus by the epithelium on the one hand, and from the evacuation of mucus through the cilia on the other hand. Finally, in Chapter 3, we studied the influence of airflow through the bronchial lumen on the efficiency of mucociliary clearance, and this, by considering a normal, strong, and extreme breathing regime

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Xie, Weiliang. "Regulators of airway submucosal glands development and functions." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/3409.

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Tracheobronchial submucosal glands (SMGs) develop from clusters of epithelial progenitor cells basally orientated within the surface airway epithelium called primordial glandular placodes (PGPs). Signal transduction events that coordinate the transitional process from PGPs into fully developed SMGs consisting of intricately branched networks of tubular secretary structures are still poorly understood. Wnt/β-catenin dependent induction of lymphoid enhancing factor-1 (Lef-1) expression in PGP progenitor/stem cells is required for SMG formation and maturation in the airway. In an effort to better understand the regulatory mechanisms that control Lef-1 during airway SMG development, I have studied its transcriptional regulation. I discovered that Sox2 expression is predominantly confined to the surface airway epithelium (SAE) and is repressed as Lef-1 is induced within PGPs. Deletion of Sox2 in polarized primary airway epithelia significantly enhances Lef-1 mRNA expression. Consequently, my hypothesis is that Sox2 functions as a negative regulator of Lef-1 expression in the SAE. I demonstrated that Sox2 modulates the expression of Lef-1 both independent and dependent on Wnt/β-catenin signaling. I discovered that a Sox2-binding site located in the Wnt Responsive Element (WRE) region of the 2.5Kb Lef-1 promoter is required for Sox2-mediated inhibition of β-catenin-dependent Lef-1 promoter transcription. It is important to understand the biology of SMG development because SMGs are the major mucus-producing structures in the proximal airway and are important in regulating the innate immunity of the lung in response to various neural signals. SMG ducts have also been proposed as a potential protective niche for slowly cycling progenitor cells (SCPCs). Hence, aberrant SMG function is thought to aggravate the pathoprogression of lung disease. Cystic fibrosis (CF) is a disease caused by a defect in the gene that encodes a chloride ion channel called cystic fibrosis transmembrane conductance regulator (CFTR). The absence of CFTR in serous cells within SMG ducts contributes to defective airway secretion, which alters the microenvironment within SMGs. I hypothesized that the glandular SCPC niche may be dysfunctional in CF. I reported that the neural peptide, calcitonin gene-related peptide (CGRP) activates CFTR-dependent SMG secretions and that this signaling pathway is hyperactivated in CF human, pig, ferret, and mouse SMGs. CFTR-deficient mice failed to maintain glandular SCPCs following airway injury, suggesting that the glandular SCPC niche may be dysfunctional in CF. CGRP levels increase following airway injury and function as an injury-inducible mitogen that stimulates progenitor cell proliferation. However, components of the receptor for CGRP (RAMP1 and CLR) were expressed in a very small subset of SCPCs, suggesting that CGRP indirectly stimulates SCPC proliferation through paracrine mechanisms. This discovery may have important implications for injury/repair mechanisms in the CF airway.

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Lynch, Thomas John. "Adult stem cells in the trachea and tracheal submucosal glands." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/6464.

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Breathing is essential for human life, yet tens of millions of people in the U.S. alone suffer from lung diseases. With each breath, lungs are exposed to the external environment. Inhaled air first passes through the trachea, bronchi, and finally the bronchioles before it reaches the alveoli where gases are exchanged. A barrier of epithelial cells protects the airways. In addition, epithelial glands also secrete protein-rich fluids onto the airway surfaces to help maintain sterility. Injury, disease, or other factors can damage these cells, and regiospecific stem cells (SCs) can divide to replace them. However, many important details about lung SCs are still unknown. For example, what processes control SC division? How do region-specific SCs differ from one another? And how does disease or injury impact SC biology? We found that some processes that regulate lung development also control adult SC division following injury. We show that SCs from airway glands give rise to surface epithelial cell types and glandular cell types. In contrast, surface SCs only generated surface cell types. Finally, we identify a type of cell in the glands that can regenerate surface cell types after severe injury. These studies provide new insights into the neighborhoods in which SCs reside in the large airways and processes that control their contribution to airway repair following injury. Overall, this research provides important new insights into adult SC biology and conditions affecting lung health.

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Частини книг з теми "Glandes submucosales"

Fung, Denis C. K., and Duncan F. Rogers. "Airway Submucosal Glands: Physiology and Pharmacology." In Airway Mucus: Basic Mechanisms and Clinical Perspectives, 179–210. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-8874-5_8.

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Shimizu, Takeshi. "Mucus, Goblet Cell, Submucosal Gland." In Nasal Physiology and Pathophysiology of Nasal Disorders, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37250-6_1.

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Shimizu, Takeshi. "Mucus, Goblet Cell, Submucosal Gland." In Nasal Physiology and Pathophysiology of Nasal Disorders, 1–14. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-12386-3_1.

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Wine, Jeffrey J., Nam Soo Joo, Jae Young Choi, Hyung-Ju Cho, Mauri E. Krouse, Jin V. Wu, Monal Khansaheb, et al. "Measurement of Fluid Secretion from Intact Airway Submucosal Glands." In Methods in Molecular Biology, 93–112. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-120-8_6.

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Filali, Mohammed, Xiaoming Liu, Ningli Cheng, Duane Abbott, Vladimir Leontiev, and John F. Engelhardt. "Mechanisms of Submucosal Gland Morphogenesis in the Airway." In Mucus Hypersecretion in Respiratory Disease, 38–50. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470860790.ch4.

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Hümmer, B., I. Purnama, and H. L. Hahn. "Effect of Bovine Surfactant on Mucus Secretion from Tracheal Submucosal Glands." In Surfactant Replacement Therapy, 319–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73305-5_37.

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Tata, Aleksandra. "Stem cells of submucosal glands: their function as tissue stem cells and a reserve population for airway repair." In Lung Stem Cells in Development, Health and Disease, 70–83. Sheffield, United Kingdom: European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10009220.

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Baraniuk, James N., Michael S. Blaiss, and Debendra Pattanaik. "Nonallergic Rhinopathies and Lower Airway Syndromes." In Asthma, 244–59. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199918065.003.0019.

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Nonallergic rhinitis is a heterogeneous disease consisting of wide variety of entities that present with persistent nasal symptoms. “United airways” has become a slogan verging on dogma. The concept gained momentum with the realization that the unifying atopic pathophysiology of the nose and tracheobronchial tree lead to coexistent allergic rhinitis and allergic asthma, respectively. Including nonallergic mechanisms and the differential diagnosis of comorbid rhinitides with reversible and irreversible lower airway obstructive entities is more problematic. Although the nose and foregut-derived tracheobronchial tree have distinct embryonic origins, they share exposure to air, pseudostratified epithelium with extensive submucosal glands, common elements of the innate and acquired mucosal immune systems, and extensive nociceptive and autonomic nervous system sensors and controls. Mechanisms affecting both anatomic sites are likely to develop comorbid disease. Anatomic differences contribute to discrete pathologic conditions, as allowed by the bony box of the nasal cavity versus the cartilaginous walls and elastic alveolar interstitial tethers for bronchi and bronchioles. The diverse pathologic states of the nasal mucosa and their relationships with bronchial hyperresponsiveness are the focus of the remainder of this discussion.

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Wass, John A. H. "Somatostatinoma." In Oxford Textbook of Endocrinology and Diabetes, 929–31. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0657.

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Somatostatin was isolated in 1973 by Paul Brazeau in Roger Guillemin’s laboratory. It was found to have a widespread distribution, not only in the hypothalamus and brain but also in the gastrointestinal tract. Sixty-five per cent of the body’s somatostatin is in the gut, mostly in the D cells of the gastric and intestinal epithelium. It is also present in the myometric and submucosal plexuses. The highest concentration is in the antrum of the stomach and there is a gradual decrease of concentrations down the gastrointestinal tract. Five per cent of the body’s somatostatin is in the pancreas. Infused somatostatin, which has a short half-life of 3 min, has a large number of actions on the pituitary gland, the endocrine and exocrine pancreas, gastrointestinal tract, other hormones, and on the nervous system (Box 6.8.1). Among its various actions of importance in the gastrointestinal tract is the inhibition of gastrin and cholecystokinin (CCK). In the pancreas, insulin and glucagon are inhibited. Nonendocrine actions include inhibition of gastric acid secretion, pancreatic exocrine function, gall bladder contraction, and intestinal motility. Intestinal absorption of nutrients, including glucose, triglycerides, and amino acids, is also inhibited (1). Somatostatin exists in two main forms, as a 14-amino acid peptide (somatostatin 14) present mainly in the pancreas and the stomach, and as a 28-amino acid peptide present mainly in the intestine. Somatostatin 14 is the peptide present in enteric neurons. Somatostatin receptors are present on many cell types, including the parietal cells of the stomach, G cells, D cells themselves, and cells of the exocrine and endocrine pancreas. A large number of tumours also have somatostatin receptors and these include pituitary adenomas, endocrine pancreatic tumours, carcinoid tumours, paragangliomas, phaeochromocytomas, small cell lung carcinomas, lymphomas, and meningiomas. Five different somatostatin receptors (SSTRs) have been cloned (SSTR1–SSTR5) and all are on different chromosomes. These have a varying affinity for somatostatin 14 and somatostatin 28 and a varying tissue distribution with SSTR2 and 5 being predominant in the pituitary (2). Somatostatin can act either as an endocrine hormone or in a paracrine or autocrine way. It probably also has luminal effects in the gastrointestinal tract. Lastly, it can act as a neurotransmitter (3).

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Тези доповідей конференцій з теми "Glandes submucosales"

Mucenski, Michael, Michael Bruno, Susan Wert, Joseph Locker, and Jeffrey Whitsett. "NKX2.8 Participates In A Regulatory Network In Submucosal Glands And Tracheal Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5495.

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Yu, W., M. Stroik, B. Hilkin, M. Rector, N. Gansemer, M. Abou Alaiwa, D. A. Stoltz, and M. Welsh. "Airway Submucosal Gland Hypertrophy in Primary Ciliary Dyskinesia Pigs." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a6419.

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Hegab, Ahmed E., Vi Luan Ha, Jennifer L. Gilbert, Derek W. Nickerson, Aik Ooi, and Brigitte N. Gomperts. "Repair And Regeneration Of The Tracheal Epithelium And Submucosal Glands After Hypoxic-Ischemic Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5294.

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Hegab, Ahmed E., Vi L. Ha, Jennifer L. Gilbert, Aik T. Ooi, Derek Nickerson, and Brigitte N. Gomperts. "Characterization And Isolation Of Cellular Subpopulations In Mouse Proximal Airway Epithelium And Submucosal Glands." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5496.

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Herrera, Ana M., Maria A. Escobar, Lina M. Salazar, and Mario A. Correa. "Vitronectin Is Expressed By Submucosal Gland Cells In The Human Airways." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2058.

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Yu, W., D. A. Stoltz, and M. Welsh. "Luminal ATP Stimulates Submucosal Gland Mucus Secretion Through the P2X4 Receptors." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1247.

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Hegab, Ahmed E., Vi Luan Ha, Bhartii Bisht, Jennifer L. Gilbert, Derek W. Nickerson, Yasser Attiga, Aik T. Ooi, and Brigitte N. Gomperts. "Isolation And Characterization Of Sphere-Forming Cells From Human Upper Airway Surface Epithelium And Submucosal Glands." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6336.

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Muramatsu, Soshi, Tsutomu Tamada, Masayuki Nara, Koji Murakami, Shigeki Chiba, Toshiaki Kikuchi, Masahito Ebina, and Toshihiro Nukiwa. "Toll-Like Receptor 5 Potentiates Ca2+-Dependent Electrolytes Secretion From Airway Submucosal Gland." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4275.

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Murakami, Koji, Tsutomu Tamda, Masayuki Nara, Toshiaki Kikuchi, Masahito Ebina, and Toshihiro Nukiwa. "Toll-like Receptor Signaling As A Potentiator In The Airway Submucosal Gland Secretion." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6451.

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Murakami, Koji, Tsutomu Tamada, Masayuki Nara, Soshi Muramatsu, Toshiaki Kikuchi, Masahiko Kanehira, Masahito Ebina, and Toshihiro Nukiwa. "Toll-Like Receptor 4 Signaling As A Potentiator In The Airway Submucosal Gland Secretion." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2056.

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