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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 752 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 752 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 238 (1974), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 206 (1980), S. 387-394 
    ISSN: 1432-0878
    Keywords: Closure ; Ileal development ; Crypt cell proliferation ; Sympathectomy ; Mitosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The present experiments were designed to investigate ileal crypt cell division before and after neonatal closure to macromolecular absorption by measurements of mitotic index, labelling index, colchicine-induced estimation of mitotic rate (mitoses/cell/hour) and crypt depth and villus height on postnatal days 15–23. In addition, the effects of the sympathetic nervous system on crypt cell proliferation were analyzed by guanethidine-induced sympathectomy. Guanethidine treatment resulted in at least a 70 % reduction in superior cervical and coeliac perikarya at 15 days after birth. All cell proliferative indices demonstrated a rather constant rate of cell division in the ileal epithelium between 15 and 17 days after birth with a sudden burst of mitotic activity on day 18. The mitotic rate of control rats increased from day 18 to 23 with 3-week-old rat demonstrating a faster rate of ileal crypt cell proliferation than adult rats. The ileal crypt depth more than doubled between 15 and 23 days while the height of the villus column increased slowly but steadily (36 %) during the period of this study. Cell division is inhibited by guanethidine-induced sympathectomy although there is still an acceleration of mitosis in the post-closure period. The relationship of sympathectomy and ileal crypt cell proliferation is discussed and compared to hormonal effects on closure and related developmental events.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 248 (1987), S. 119-123 
    ISSN: 1432-0878
    Keywords: Odontoblasts ; Protein synthesis ; Denervation ; Neural regulation ; Wound healing ; Autoradiography ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Odontoblasts respond to occlusal trauma by increased elaboration of a matrix which is subsequently calcified to form reparative dentin. The purpose of the present study was to analyze quantitatively and compare the ability of odontoblasts to synthesize collagen after wounding in rats with an intact innervation (baseline) and in rats with sensory (inferior alveolar nerve, IAN) and/or sympathetic (superior cervical ganglion, SCG) surgical denervation. Surgery was performed 7 days prior to wounding. All rats had 1 mm of enamel and dentin removed from the occlusal surface of the first mandibular molar (resected side) with the contralateral tooth serving as a control. Rats were killed 1 h after injection with3H-proline on days 0, 5, 10 or 15 after wounding, and mandibles were removed and processed for autoradiography. Grain counts were performed over odontoblasts throughout the pulp horns for each time period and for control and experimental molars in intact (baseline) and denervated groups. When compared to the control baseline, the experimental baseline data showed increased3-proline uptake throughout the study with a peak at 5 days. When compared to the baseline data, IAN and SCG results demonstrated a delay or attenuation of the protein synthetic response. The results indicate that the sensory and sympathetic neural components may regulate odontoblastic response to wounding.
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cell & tissue research 195 (1978), S. 239-250 
    ISSN: 1432-0878
    Keywords: Guanethidine ; Chemical sympathectomy ; Intestinal epithelium ; Cell proliferation ; Cell cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Guanethidine-induced sympathectomy in the rat during the neonatal period (injection of 20 μg/g body weight every 48 h from day of birth until day 14) produces an absolute reduction in the number of sympathetic ganglion cells, but no significant alteration of body weight. Superior cervical ganglia show 79.8 % fewer cell bodies at 15 days and 92.3 % at 45 days; coeliac ganglia exhibit an 81.0 % reduction at 15 days and 89.6 % at 45 days in guanethidine-treated rats as compared to normal controls. The sympathetic ganglion cells that remain after treatment have an abnormal morphological appearance with distended mitochondria and depletion of endoplasmic reticulum. Sympathectomy produces a prolongation of the generation cycle time (Tc) as measured by the colchicine-induced mitotic arrest technique, and a decrease in labelling, mitotic, and migration indices. In addition, sympathectomy suppresses the amplitude of the circadian rhythm in mitotic activity. The general suppression of this activity in the intestinal epithelium is more pronounced in the jejunum and ileum than in the duodenum. Variation in the effectiveness of sympathectomy on the inhibition of intestinal cell proliferation may be related to segmental differences in cell proliferation, to segmental differences in innervation, and/or to segmental variation in the effectiveness of guanethidine.
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  • 7
    Electronic Resource
    Electronic Resource
    New York, NY : Wiley-Blackwell
    Journal of Supramolecular Structure and Cellular Biochemistry 15 (1981), S. 219-234 
    ISSN: 0275-3723
    Keywords: collagen ; SLS ; phospholipid ; surfactant ; fibrillogenesis ; dipalmitoyl phosphatidyl choline ; electrostatic interactions ; Chemistry ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The effect of dipalmitoyl phosphatidyl choline (DPPC), the major phospholipid component of pulmonary surfactant, on the precipitation of collagen in the form of native fibrils and segment-long-spacing (SLS) aggregates was studied in vitro. The effects of DPPC on both phases of collagen fibrillogenesis were analyzed spectrophotometrically, and alterations in the morphology of precipitated fibrils and SLS aggregates were ascertained by transmission electron microscopy (TEM). Low concentrations of DPPC inhibited the growth phase of fibrillogenesis, while higher concentrations were required to inhibit nucleation. Both the meshwork density and mean width of precipitated fibrils were altered by DPPC, as was the size of SLS aggregates. Segment-long-spacing aggregates prepared from pepsin-treated collagen were inhibited to a greater degree than SLS aggregates prepared from untreated collagen, indicating that the pepsin-susceptible residues of the telopeptide extensions of tropocollagen molecules stabilize SLS aggregates against the effects of DPPC. Based on these results and the inhibition of the growth phase at lower concentrations than those which inhibited the nucleation phase of fibrillogenesis, it was concluded that the primary mechanism of DPPC inhibition is electrostatic interference between the positively charged phospholipid molecules and the net positive charge of collagen. It is proposed that pathological conditions involving the pulmonary epithelium may allow interaction between surfactant and collagen, which could further weaken the interstitial connective tissue.
    Additional Material: 9 Ill.
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  • 8
    ISSN: 0263-6484
    Keywords: Atrial natriuretic peptides ; rats ; fetal development ; neonate ; immunochemistry ; hormone receptors ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: To assess the possibility that atrial natriuretic peptide plays a role in salt and water balance during early mammalian development, we examined hearts from fetal and neonatal rates for the presence of this peptide and presumed target tissues for their ability to bind the hormone. Immunohistochemistry was used to localize and radioimmunoassay to quantify this peptide in heart. Immunoreactive artrial natriuretic peptide was visualized in the fetal heart on day 17·5 post-conception. It was distributed throughout the atrial appendages and free wall and, in ventricle, in the trabeculae carnae and chordae tendineae. The concentrations of immunoreactive atrial natriuretic peptide in atria of rats on day 19·5 post-conception were one-tenth of those in the adult. Levels of this peptide in fetal ventricle were low and virtually absent from the adult tissue. Specific binding of radiolabelled atrial natriuretic peptide measured by whole organ counting occurred in several organs from 19·5-day fetal and neonatal rats. A number of these tissues, including the kidney, ileum, adrenal, lung and liver, are targets for and/or bind the peptide in adult rats. Specific binding in these tissues was localized using autoradiography at anatomical sites similar to those in adult organs. Specific binding was also seen in fetal but not neonatal skin. In the kidney, binding was associated with immature as well as mature glomeruli. These findings support the proposition that atrial natriuretic peptide may function in the perinatal rat as it does in the adult and, in addition, may play a unique role during fetal life.
    Additional Material: 6 Ill.
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  • 9
    Publication Date: 1978-12-01
    Print ISSN: 0302-766X
    Electronic ISSN: 1432-0878
    Topics: Biology , Medicine
    Published by Springer
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  • 10
    Publication Date: 1987-04-01
    Print ISSN: 0302-766X
    Electronic ISSN: 1432-0878
    Topics: Biology , Medicine
    Published by Springer
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