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  • 1
    Electronic Resource
    Electronic Resource
    Association between inflammation and epithelial damage-restitution processes in allergic airways in vivo (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Associations between allergen challenge-induced sites of epithelial damage and the distribution of leucocytes and extravasated plasma remain unexplored.Objective To study neutrophils, eosinophils, and fibrinogen at allergen challenge-induced patchy epithelial damage-restitution sites in guinea-pig trachea.Methods After local challenge tracheal tissue (cryo sections and whole-mounts) and lumen (selective tracheal lavage) were examined at 1, 5, and 24 h. Eosinophils, neutrophils and fibrinogen were identified by histochemistry.Results Neutrophils increased markedly in tracheal lavage fluids and in tissue and were strongly associated with the challenge-induced epithelial craters of damage-restitution. At 1 and 24 h eosinophils were increased in the tracheal lumen whereas the surrounding tissue displayed a reversed pattern. Gels rich in fibrinogen, neutrophils, and eosinophils were present in epithelial crater areas, protruding into the lumen. Clusters of free eosinophil granules, Cfegs, released through lysis of eosinophils, and neutrophils with long cytoplasmatic protrusions abounded in these crater areas.Conclusions The present findings provide important new insights into allergic airways where sites of epithelial damage-restitution processes emerge as the major loci for eosinophil, neutrophil, and plasma protein activities, the latter likely causing leukocyte adhesion and activation in vivo. The disttibution of eosinophils in this study suggests roles of these cells both in airway mucosa and in regional lymph nodes. Based on the present study we also propose that lysis of eosinophils and Cfegs generation are a major paradigm for activation of these cells in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1997.tb01181.x
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  • 2
    Electronic Resource
    Electronic Resource
    Epithelial shedding—restitution as a causative process in airway inflammation (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 26 (1996), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1996.tb00604.x
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  • 3
    Electronic Resource
    Electronic Resource
    Epithelial pathways for luminal entry of bulk plasma (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inflammatory challenges of the airway mucosa cause luminal entry of bulk plasma. Extravasation of plasma is well described but the routes for epithelial passage of plasma are largely unknown. Using colloidal gold (5 nm) as tracer we have now examined the fate of extravasated plasma in the airways. The tracer was given intravenously to anaesthetized, ovalbumin-sensitized guinea-pigs 2min prior to airway mucosal challenge with 12pmol ovalbumin (the dose was selected from a separate dose-response study). Tissue specimens were collected 30s, 3 and 6 min after end of challenge (separate time course experiments suggested that the peak rate of entry of plasma occurred at about 5 min). The colloidal gold particles were visualized by autometallographic silver intensification. The gold produced no circulatory disturbance and had a uniform vascular distribution with negligible adherence to vascular endothelium. After challenge gold was first widely distributed in the lamina propria. At 3 and 6 min the tracer was also in the epithelium and airway lumen. It appeared that plasma was moved distinctly between and all around each epithelial cell. Bright field-, scanning-, and transmission electron-microscopy indicated that the luminal entry of plasma did not affect the integrity of the epithelial lining. This study demonstrates that the plasma exudate moves across an intact epithelial layer through ubiquitous paracellular pathways. Even at a pronounced acute plasma exudation response exceedingly small amounts of plasma may pass around a single cell explaining the non-injurious nature of mucosal exudation of bulk plasma in health and disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb01025.x
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  • 4
    Electronic Resource
    Electronic Resource
    Airway permeability (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 25 (1995), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.1995.tb00022.x
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  • 5
    Electronic Resource
    Electronic Resource
    Prompt epithelial damage and restitution processes in allergen challenged guinea-pig trachea in vivo (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical & experimental allergy 27 (1997), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Little is known about the induction and the morphology of epithelial damage, and of the ensuing epithelial restitution processes in allergic airways.Objective To examine epithelial damage and restitution in allergen challenged guinea-pig trachea.Methods Whole-mount techniques, transmission and scanning electron microscopy, cryosectioning, and histochemical staining were used. Cell proliferation was monitored by BrdU-immunohistochemistry.Results Allergen challenge produced patchy, crater-like, and leucocyte-rich epithelial damage sites. At 1, 5, and 24 h damage was associated with poorly differentiated epithelial restitution cells. Already at 1 h the epithelial craters had a floor of flattened restitution cells and the damaged areas comprised 〈 1% of the mucosal surface area (whole-mount preparations). In contrast, cryo sections displayed large areas (∼ 20%, 1 h) of denudation. Epithelial, and subepithelial (fibroblasts, smooth muscle) proliferation was increased 5 and 24 h after challenge (P 〈 0.01).Conclusion Within 1 h allergen challenge has induced patchy damage sites where epithelial restitution is already advanced; although easily produced by cryosectioning frank denudation was not evident in whole-mount preparations. The present findings may explain the well maintained, functional tightness of allergic airways displaying epithehal damage, shedding, and even denudation. The present data also suggest the possibility that epithelial damage-restitution may be causative to allergic airway remodelling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2222.1997.1200932.x
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  • 6
    Electronic Resource
    Electronic Resource
    Pituitary Adenylate Cyclase-Activating Peptide in Sensory and Autonomic Ganglia: Localization and Regulation (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 805 (1996), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb17501.x
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  • 7
    Electronic Resource
    Electronic Resource
    Epithelium, microcirculation, and eosinophils – new aspects of the allergic airway in vivo (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 52 (1997), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1997.tb00989.x
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  • 8
    Electronic Resource
    Electronic Resource
    Developmental expression of neuronal and endocrine markers in the parathyroid glands of the rat (1997)
    Springer
    Anatomy and embryology 195 (1997), S. 515-524 
    Details
    ISSN: 1432-0568
    Keywords: Key words Ontogeny ; Parathyroid gland ; Neuropeptides ; Chromogranin ; mRNA expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The parathyroid glands of the adult rat harbor a number of neuroendocrine markers, biologically active peptides and ”classical” neuromessengers in addition to parathyroid hormone (PTH). Their appearance during parathyroid development is, however, not known. In the present study we have examined several neuroendocrine markers and neuromessengers in the parathyroid glands of the developing rat [embryonic stage 21(E21), newborn, 1, 2, 3, 4 week old, and adult rats] using immunocytochemistry. Chromogranin A- and PTH-mRNA were also examined by in situ hybridization and the mRNA levels were quantitated by computerized image analysis. Protein gene product 9.5- and synaptophysin-containing nerve fibers appeared already before birth and then gradually increased in number postnatally, and at the age of 4 weeks the nerve fibers were moderate in number to numerous. Nerve fibers containing calcitonin gene-related peptide, neuropeptide Y and vasoactive intestinal polypeptide also increased gradually in number, while galanin- , substance P- and tyrosine hydroxylase-containing fibers remained few throughout development. The glandular cells expressed chromogranin A, pancreastatin and PTH already before birth. The levels of chromogranin A- and PTH-mRNA were low at E21 and increased markedly at birth; chromogranin A mRNA levels had increased even more at 1 week postnatally. Three to 4 weeks after birth the levels of PTH- and chromogranin A mRNA again increased, then stabilized at a slightly lower level in the adult rat. Our findings demonstrate that the parathyroid glands of rat are already innervated and express PTH and chromogranin A before birth and that the density of peptide-containing nerve fibers changes during development. The stepwise increases of PTH- and chromogranin A mRNAs during development indicate marked changes in parathyroid activity occurring at birth and at weaning.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004290050071
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  • 9
    Electronic Resource
    Electronic Resource
    Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat islets following dexamethasone treatment (1995)
    Springer
    Diabetologia 38 (1995), S. 395-402 
    Details
    ISSN: 1432-0428
    Keywords: Islet amyloid polypeptide ; amylin ; insulin ; dexamethasone ; rat ; pancreatic islets ; in situ hybridization ; gene expression ; mRNA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP), a novel islet hormone candidate, has been reported to be over-expressed relative to insulin in rats following dexamethasone treatment. In order to investigate the expression of IAPP and insulin following dexamethasone treatment of rats for 12 days, we applied in situ hybridization and immunocytochemistry, allowing us to evaluate islet changes in gene expression and morphology. Tissue concentrations of IAPP and insulin were measured by radioimmunoassay. A low dose of dexamethasone (0.2 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 249±13% and 150±24% of controls, respectively (p〈0.001 and p〈0.01). A high dose of dexamethasone (2.0 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 490±13% and 203±9% of controls, respectively (p〈0.001 and p〈0.001). The pancreatic concentration of IAPP increased more than that of insulin (p〈0.05). Morphometric analysis revealed that dexamethasone treatment induced both hyperplasia and hypertrophy of insulin cells. Changes in the cellular localization of IAPP and insulin mRNA were not observed. Thus, we conclude that the increased level of IAPP mRNA is due to both an increase at the cellular level as well as hyperplasia/hypertrophy of insulin cells. In contrast, the increased level of insulin mRNA appears to be due to hyperplasia/hypertrophy of insulin cells, since insulin gene expression decreased at the cellular level (p〈0.001 vs controls). These observations provide further evidence that IAPP and insulin gene expression are regulated in a non-parallel fashion, which may be relevant to the pathogenesis of non-insulin-dependent diabetes mellitus
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410276
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  • 10
    Electronic Resource
    Electronic Resource
    Non-parallelism of islet amyloid polypeptide (amylin) and insulin gene expression in rat islets following dexamethasone treatment (1995)
    Springer
    Diabetologia 38 (1995), S. 395-402 
    Details
    ISSN: 1432-0428
    Keywords: Key words Islet amyloid polypeptide ; amylin ; insulin ; dexamethasone ; rat ; pancreatic islets ; in situ hybridization ; gene expression ; mRNA.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide (IAPP), a novel islet hormone candidate, has been reported to be over-expressed relative to insulin in rats following dexamethasone treatment. In order to investigate the expression of IAPP and insulin following dexamethasone treatment of rats for 12 days, we applied in situ hybridization and immunocytochemistry, allowing us to evaluate islet changes in gene expression and morphology. Tissue concentrations of IAPP and insulin were measured by radioimmunoassay. A low dose of dexamethasone (0.2 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 249 ± 13 % and 150 ± 24 % of controls, respectively (p 〈 0.001 and p 〈 0.01). A high dose of dexamethasone (2.0 mg/kg daily) increased the islet levels of IAPP and insulin mRNA to 490 ± 13 % and 203 ± 9 % of controls, respectively (p 〈 0.001 and p 〈 0.001). The pancreatic concentration of IAPP increased more than that of insulin (p 〈 0.05). Morphometric analysis revealed that dexamethasone treatment induced both hyperplasia and hypertrophy of insulin cells. Changes in the cellular localization of IAPP and insulin mRNA were not observed. Thus, we conclude that the increased level of IAPP mRNA is due to both an increase at the cellular level as well as hyperplasia/hypertrophy of insulin cells. In contrast, the increased level of insulin mRNA appears to be due to hyperplasia/hypertrophy of insulin cells, since insulin gene expression decreased at the cellular level (p 〈 0.001 vs controls). These observations provide further evidence that IAPP and insulin gene expression are regulated in a non-parallel fashion, which may be relevant to the pathogenesis of non-insulin-dependent diabetes mellitus [Diabetologia (1995) 38: 395–402]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410276
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