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  • 1
    Electronic Resource
    Electronic Resource
    Lung development and the pulmonary surfactant system: Hormonal influences (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 198 (1980), S. 13-34 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The effect of hormones on developmental events is not a new area of scientific investigation. However, in the last decade, the developing lung has been the focus of an increasing amount of basic and applied research. Inadequate development of the newborn's respiratory system precludes extrauterine existence; indeed, such respiratory inadequacy has been a leading cause of death in premature infants. Tremendous strides have been made in understanding the basic cell biology of the developing lung. Much has been learned about the source, composition, and function of pulmonary surfactant, a surface-active material produced by the lung and essential to alveolar stability. Deficient stores of this material is a major etiologic factor in the respiratory distress syndrome of the newborn (RDS). This fact, coupled with observations that certain hormones can accelerate lung development and the consequent availability of adequate stores of pulmonary surfactant, has led to a large body of literature dealing with the effects of hormones (and other agents) on lung development. It is the purpose of this literature review (1) to discuss the various kinds of investigations which have linked surfactant synthesis to the type II pulmonary epithelial cell; and (2) to review the current status of research dealing with the effects of glucocorticoids and thyroid hormons on lung maturation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091980103
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  • 2
    Electronic Resource
    Electronic Resource
    Hormones and the lung. I. Thyroid hormones and glucocorticoids in lung developmentThis study was supported by Grant HL15316 from the National Heart, Lung and Blood Institute, N.I.H. Portions of this work were presented at the Ninety-first meeting of the American Association of Anatomists, Vancouver, British Columbia. (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 194 (1979), S. 15-39 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: It has been proposed that thyroid hormones may have a role in the regulation of lung development and the maturation of the surfactant system. The purpose of this study was to examine the effects of exogenous thyroxine (T4) on rat lung development and to investigate possible interactions of this hormone with the glucocorticoids, other hormones implicated in the regulation of lung development.A number of different experimental protocols were utilized: T4 was administered to day 17 and 18 rat fetuses from untreated animals as well as from animals which had been adrenalectomized or treated with the 11-β-hydroxylase inhibitor, Metopirone; replacement hydrocortisone was administered to some groups. Sham-operated and untreated animals were included as controls. Animals were sacrificed from days 19-22 (term, day 22-23) of gestation and the fetal lungs were examined. Accelerated lung development was observed in all experimental groups receiving T4. Alveolar epithelial cells were more differentiated in comparison to controls. Glycogen deposits were diminished, cell flattening was more advanced, mitochondria, Golgi complexes and rough endoplasmic reticulum were more prominent, and lamellar bodies, storage sites for pulmonary surfactant, were greatly increased in number. Secretion of lamellar bodies into the alveolar space was also stimulated. The results also indicated that T4 and glucocorticoids act together in the acceleration of lung development. Under conditions of decreased glucocorticoids (Metopirone treatment and adrenalectomy), stimulatory effects of T4 were still evident but less pronounced; hydrocortisone replacement increased the observed stimulation. Maximal acceleration of lung development was observed subsequent to T4 and uncontrolled surgical stress. These results demonstrate that T4 can accelerate rat lung development and that this acceleration is maximal in the presence of glucocorticoids.
    Additional Material: 15 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091940103
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Hormones and the lung II. Immunohistochemical localization of thyroid hormone binding in type II pulmonary epithelial cells clonally-derived from adult rat lungThis study was supported by Grants HL15316, HL21008, HL19513 from the National Heart, Lung And Blood Institute, N.1.H and Grant R-274 from the United Cerebral Palsy Education and Research Foundation. Preliminary results were presented at the Ninetieth meeting of the American Association of Anatomists, Detroit, Michigan. (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 195 (1979), S. 611-619 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The type II pulmonary epithelial cell is the recognized site of surfactant synthesis and storage. Results of recent studies indicate that the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), may be important regulators of surfactant production and/or release. Direct and indirect immunofluorescence techniques were used in an attempt to demonstrate binding of T3 and T4 in monolayer cultures of isolated type II cells. These cultured epithelial cells are clonally-derived from adult rat lung, retain a diploid karyotype through 35 population doublings in vitro, contain granular inclusions (lamellar bodies) in the perinuclear cytoplasm, and synthesize phosphatidylcholine via the CDP-choline pathway.In isolated type II cells, either of two fluorescent patterns was observed: (a) nuclear fluorescence accompanied by a reticular perinuclear network; or (b) diffuse cytoplasmic accumulations with concentrations around perinuclear cytoplasmic inclusions. Ultrastructurally these inclusions had the typical appearance of lamellar bodies. Histochemical studies demonstratedthat these inclusions contained surfactant-associated nonspecific esterases and stained with Nile blue hydrochloride. The positive reactions with these two recognized markers for pulmonary surfactant indicate that these inclusions are indeed lamellar bodies, the putative sites of surfactant synthesis and/or storage. These findings suggest that the type II pulmonary epithelial cell contains specific binding sites for thyroid hormones, and support the hypothesis that thyroid hormones are regulators of surfactant metabolism.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091950404
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    Paper (German National Licenses)
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