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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 29 (1957), S. 939-941 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 62 (1940), S. 1368-1371 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. ; Stafa-Zurich, Switzerland
    Materials science forum Vol. 321-324 (Jan. 2000), p. 960-964 
    ISSN: 1662-9752
    Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Surgical and radiologic anatomy 14 (1992), S. 335-339 
    ISSN: 1279-8517
    Keywords: Paranasal sinuses ; Postnatal development ; Radiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Le développement des sinus para-nasaux ou sinus accessoires commence très précocement dans la vie in-utéro. Chez le nouveau-né le sinus ethmoïdal, qui contrôle l'apparition de tous les autres sinus, et le sinus maxillaire peuvent déjà être identifiés à la radio. Le sinus frontal a la forme d'un triangle a l'âge de 4 ans et franchit la ligne supra-orbitaire à 6 ans. Le sinus sphénoïdal commence à creuser le cornet sphénoïdal dès l'âge de 4 ans et devient visible à la radio à 8 ans lorsqu'il s'étend jusqu'à la fosse hypophysaire. Chez l'enfant de 12 ans tous les sinus ont pratiquement atteint leur taille adulte. Cependant la taille et la forme de ces sinus et spécialement les sinus frontaux et sphénoïdaux sont très différentes.
    Notes: Summary The development of the paranasal or accessory sinuses begins very early in utero. In the newborn the ethmoidal sinus, which gives rise to all the other sinuses, as well as the maxillary sinus, can already be identified on x-rays. The frontal sinus appears as a triangle at the age of four and oversteps the supraorbital margin at the age of six. The sphenoidal sinus begins to excavate the concha sphenoidalis at the age of four and can be seen on x-rays at the age of eight, when it extends to the hypophyseal fossa. In the twelve-year-old child all sinuses almost reach their final sizes. However, the size and shape of all sinuses, particularly of the frontal and the sphenoidal sinuses are very different.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1279-8517
    Keywords: Paranasal sinuses, anatomy ; Paranasal sinuses, childhood ; Paranasal sinuses, MR-Imaging ; Sphenoid bone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Afin de démontrer les aspects fondamentaux du développement du sinus sphénoïdal pendant l'enfance, nous avons revu l'aspect en IRM du sinus sphénoïdal de 401 patients agés de moins de 15 ans. L'étude de la moelle osseuse, le développement de la pneumatisation, la croissance et le cloisonnement du sinus sphénoïdal ont été explorés en séquences pondérées en T1 et en T2. Le sinus sphénoïdal se présente, en séquence pondérée en T1, avec un signal faible et uniforme (moelle osseuse rouge) chez tous les enfants agés de moins de 4 mois. Ce signal hypo-intense devient hyper-intense (transformation de la moelle osseuse) à partir du 4 ème mois. Le début de la pneumatisation est noté à 13–15 mois. A l'âge de 43–48 mois, la partie antérieure du sinus sphénoïdal est pneumatisée chez 85 % des enfants. La pneumatisation est complète chez tous les patients agés de plus de 10 ans. La croissance dans chaque direction de l'espace est caractéristique. L'apparition d'un septum médian est observée à une fréquence variable par tranche d'âge, avec un maximum de 77 %. Les variations existent dans 4,5 % à 20 % des cas. La connaissance de ce phénomène peut servir de référence pour évaluer le développement normal et anormal du sinus sphénoïdal et être d'un grand intérêt dans le diagnostic et le traitement des affections du sinus sphénoïdal et des régions voisines chez l'enfant.
    Notes: Summary To obtain baseline standards of normal age-related development of the sphenoid sinus during childhood magnetic resonance images of the sphenoid sinus in 401 patients less than 15 years old were reviewed. T1-weighted sagittal and T2-weighted axial scans were evaluated for bone marrow conversion, development of pneumatization, spatial enlargement and septation of the sphenoid sinus. The sphenoid sinus had a uniformely low signal intensity (red bone marrow) on T1-weighted images in all children less than 4 months old. Signal intensity changes from hypo- to hyperintense (bone marrow conversion) started at age of 4 months. Onset of pneumatization was observed in 12% of the patients at age 13–15 months. By age 43–48 months, 85% of the patients showed pneumatization of the anterior part of the sphenoid bone. Pneumatization was complete in all patients older than 10 years. Enlargement of the sinus showed a characteristic profile in each dimension. Median septation was observed irregularly with age, with a maximum of 77%. Septum variants were noticed between 4.5% and 20%. The recognition of this phenomenon may serve as a reference for evaluating normal and abnormal development of the sphenoid sinus and may be of great value for diagnostic and therapeutic management of pathologic conditions of the child's sphenoid sinus and its surrounds.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; renin angiotensin system ; angiotensinase A
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary One of the characteristics of early diabetic nephropathy is glomerular hyperfiltration and hyperperfusion. Many factors have been suggested to induce glomerular hyperperfusion among which are an increased production of vasodilatory prostanoids, an increased synthesis of nitric oxide, a reduced responsiveness of afferent glomerular arterioles to vasoconstrictor stimuli due to diabetic metabolic disturbances and a decreased receptor density for angiotensin II. It has been known for years that angiotensin II is formed locally due to the local activation of the renin angiotensin system. The local angiotensin II concentration, however, is not only regulated by the synthesis rate but also by the local degradation through activation of an aminopeptidase. The main finding of the present study was that the mRNA expression and activity of the angiotensin II degrading enzyme, angiotensinase A, was increased twofold in diabetic rats at 5 weeks and that the increase in mRNA expression was suppressed by insulin therapy and short-term treatment with the angiotensin II antagonist saralasin, whereas angiotensinase A enzyme activity was only reduced by saralasin and not by insulin. These results demonstrate that the angiotensin II degrading exopeptidase angiotensinase A is activated in diabetic glomeruli. This increased activity may be an additional mechanism to explain glomerular hyperfiltration and hyperperfusion in early diabetic nephropathy. [Diabetologia (1996) 39: 275–280]
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Glucagon ; Enteroglucagon ; Intestinal mucosa ; Intestinal hormones ; Enterochromaffine cells ; Electron microscopy of gastrointestinal mucosa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé L'étude au microscope électronique de l'intestin de rat à différents niveaux: estomac, duodénum, jéjunum et iléon, permet d'observer 2 types de cellules à granulations denses. Le premier type, dont les granulations sont rondes, est semblable aux cellules A du pancréas. Le deuxième type de cellules, dont les granulations sont polymorphes, est associé aux cellules dites entérochromaffines. Sur la base de ce critère morphologique, et des données biochimiques affirmant l'existence dans l'intestin d'une substance biologiquement et immunologiquement proche du glucagon, il est proposé de situer la synthèse et sécrétion du glucagon intestinal au niveau de ces cellules endocrines intestinales de type A.
    Abstract: Zusammenfassung Bei einer systematischen Untersuchung der Magen-Darm-Schleimhaut mit Hilfe des Elektronenmikroskopes wurden zwei Arten von besonderen Zellen in deren Epithelien festgestellt, die mögliche Träger endokriner Tätigkeit sind. Beide sind durch elektronenoptisch dunkle Granula gekennzeichnet. Der erste Typ enthält runde Einschlüsse, die den Sekret-Granula der endokrinen A-Zellen des Pankreas sehr ähnlich sind. Der zweite Zelltyp weist auffallend polymorphe Sekretgranula auf, die derjenigen der sogenannten enterochromaffinen Zellen im Lichtmikroskop entsprechen dürften. Diese morphologische Eigenschaft sowie die biochemischen Beobachtungen, welche auf das Vorhandenscin einer dem Glucagon biologisch und immunologisch ähnlichen Substanz im Darm deuten, lassen die Annahme zu, daß die den pankreatischen A-Zellen ähnlichen Zellen für die Sekretion des Darm-Glucagons verantwortlich sind.
    Notes: Summary The gastro-intestinal mucosa of the rat has been systematically studied with the electron-microscope at the following levels: gastric fundus, pylorus, duodenum, jejunum and ileum. Two types of non-digestive epithelial cells have been observed, both exhibiting electron-dense granulations, both candidates for endocrine activity. The first type of cells contains round granules bearing remarkable similarity to the granules of pancreatic endocrine A cells. The second cell type is characterised by strikingly polymorphic granulations and would appear to correspond to the so-called enterochromaffine cells of light-microscopy. On the basis of this morphological criterion, and of the biochemical evidence suggesting the existence of a substance in the intestine which greatly resembles glucagon, biologically and immunologically, it is proposed that this substance is secreted by the first type of cells which resemble the pancreatic A cells.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy, cyclin-dependent kinase inhibitors, glomerular hypertrophy, cell cycle arrest, angiotensin II, progression of renal failure.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Renal hypertrophy occurs early in diabetes mellitus and precedes the development of glomerulosclerosis and tubulointerstitial fibrosis. We have previously shown that cultured mesangial cells exposed to high glucose are arrested in the G1-phase of the cell cycle and undergo cellular hypertrophy. High glucose-mediated induction of p27Kip1, an inhibitor of cyclin-dependent kinases, is essential in this process. Further investigations have also shown that p27Kip1 and p21Cip1, other cyclin-dependent kinase inhibitors, are up regulated in the kidneys of mice with Type I (insulin-dependent) as well as Type II (non-insulin-dependent) diabetes mellitus. Our study was undertaken to test a potential effect of short-term treatment with the angiotensin-converting enzyme inhibitor enalapril on the glomerular expression of the cyclin-dependent kinase inhibitors p16INK4, p21Cip1, and p27Kip1 in BBdp rats, an autoimmune model of Type I diabetes.¶Methods. We evaluated p16INK4, p21Cip1, and p27Kip1 protein expression in isolated glomeruli by western blots. We also assessed p27Kip1 positive glomerular cells by immunohistochemistry.¶Results. Glomerular expression of all three cyclin-dependent kinase inhibitors were stimulated in BBdp rats compared with non-diabetic BBdr animals. Enalapril treatment for 3 weeks, started after the onset of diabetes, reduced the glomerular expression of p16INK4 and p27Kip1 but not of p21Cip1. Enalapril also prevented the increase in kidney weights observed in BBdp rats but had no effect on systolic blood pressure or glucose concentrations.¶Conclusion/interpretation. Our data show that enalapril attenuates the glomerular expression of cyclin-dependent kinase inhibitors in diabetes and suggest a molecular mechanism of how angiotensin-converting enzyme inhibitors prevent renal hypertrophy in diabetes. [Diabetologia (1999) 42: 1425–1432]
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0509
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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