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PARATHYROID HORMONES --- CARTILAGE, ARTICULAR --- CHONDROCYTES - METABOLISM --- CELL, CULTURED --- HUMAN --- BELGIUM --- PARATHYROID HORMONES --- CARTILAGE, ARTICULAR --- CHONDROCYTES - METABOLISM --- CELL, CULTURED --- HUMAN --- BELGIUM
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RADIOIMMUNOASSAY --- CALCITONIN --- PARATHYROID HORMONES --- CALCIUM --- PHOSPHATES --- DISEASE --- BLOOD --- BLOOD --- RADIOIMMUNOASSAY --- CALCITONIN --- PARATHYROID HORMONES --- CALCIUM --- PHOSPHATES --- DISEASE --- BLOOD --- BLOOD
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CALCIUM --- PARATHYROID HORMONES --- CALCITONIN --- EXERTION --- PHOSPHATES --- BLOOD --- BLOOD --- BLOOD --- BLOOD --- CALCIUM --- PARATHYROID HORMONES --- CALCITONIN --- EXERTION --- PHOSPHATES --- BLOOD --- BLOOD --- BLOOD --- BLOOD
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OSTEOPOROSIS, POSTMENOPAUSAL --- VITAMIN D --- PARATHYROID HORMONES --- FRACTURES --- BLOOD --- BLOOD --- OSTEOPOROSIS, POSTMENOPAUSAL --- VITAMIN D --- PARATHYROID HORMONES --- FRACTURES --- BLOOD --- BLOOD
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Osteoporosis --- Parathyroid Hormones --- Prostaglandins E --- Fluorides --- Osteoporosis --- Somatotropin --- Ostéoporose --- Somatotrophine --- drug therapy. --- therapeutic use. --- therapeutic use. --- therapeutic use.
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Vrouwelijke vissen zetten een aanzienlijke hoeveelheid schildklierhormoon (TH) af in de eidooier. Er wordt aangenomen dat deze ruime stock aan TH gebruikt wordt door het ontwikkelende embryo zolang zijn eigen schildklier nog niet actief is. Er werd echter nog nooit aangetoond hoe belangrijk die maternale THs eigenlijk zijn en welke rol ze spelen tijdens de ontwikkeling van de embryo’s. We hebben daarom via een multidimensionale aanpak geprobeerd een antwoord te vinden op deze vraag, gebruikmakend van de zebravis als modelorganisme. Eerst hebben we de schildklierstatus van zebravisembryo’s verhoogd via een continue toediening van T3 in het groeimedium. Deze T3 supplementatie versnelde de embryonale ontwikkeling, het ontluiken en de pigmentatie, wat suggereert dat THs een stimulerende invloed uitoefenen op de embryonale ontwikkeling. Deze wijzigingen gingen gepaard met een stijging in de transcriptie van schildklierhormoonreceptor α (TRα) en een daling in de type 2 dejodase (D2) in de T3 behandelde embryo’s. Dit toont aan dat vissenembryo’s de beschikbare hoeveelheid TH kunnen regelen via aanpassing in de dejodasen en de uiteindelijke TH activiteit via aanpassen van de TR niveaus. Vervolgens probeerden we parentale hypothyroïdie te induceren om de afzetting van TH in de eieren te verminderen en de effecten hiervan na te gaan op de ontwikkeling van de embryo’s. Hiertoe behandelden we volwasen zebravissen gedurende 8 weken met het goitrogeen PTUrea. Naarmate de behandeling vorderde, verminderde de eileg echter en stopte uiteindelijk volledig. Een langdurige behandeling met goitrogenen tast blijkbaar de voortplantingscapaciteit aan met als gevolg dat slechts een klein aantal embryo’s kon worden verzameld. De mRNA expressie van dejodasen en van TRs in deze embryo’s was niet beïnvloed, mogelijks omdat de embryonale schildklierstatus niet of onvoldoende gewijzigd was. Tenslotte hebben we gebruik gemaakt van morpholino knock-down van D1 and D2 om na te gaan wat de gevolgen zijn van het onderdrukken van intracellulaire TH activatie op de embryonale ontwikkeling van zebravissen. Knock-down van D2, maar niet van D1, veroorzaakte een duidelijke vertraging in verschillende ontwikkelingsparameters. Dit toont aan dat de embryonale ontwikkeling bij zebravissen inderdaad afhankelijk is van intracellulaire TH activatie en dat dit process hoofdzakelijk gecontroleerd wordt door D2. De rol van D1 hierbij blijkt gering en treedt waarschijnlijk pas naar voor wanneer D2 geïnhibeerd wordt. Gecombineerde knock-down van zowel D1 als D2 resulteerde in opvallende defecten in de ontwikkeling en afwijkingen, wat aantoont dat het volledig blokkeren van ORD activiteit nefast is voor het ontwikkelende embryo. De significante verlaging van de TRβ transcriptieniveaus in D2 knock-down embryo’s alsmede het feit dat T3, maar niet T4, in staat was de negatieve invloed op de ontwikkeling te compenseren, geeft duidelijk aan dat de waargenomen effecten het gevolg waren van een lokaal tekort aan T3 in het embryo. De gedeeltelijke klonering van zebravis D3 en de daaropvolgende ontogenetische expressiestudie toonden aan dat het TH inactiverende enzym D3 tot expressie komt vanaf het begin van de embryonale ontwikkeling en sterk reageert op T3 supplementatie. We kunnen tot slot stellen dat de versnelde ontwikkeling bij verhoogde schildklierstatus en de vertraging in ontwikkeling bij een tekort aan THs samen met de actieve rol van de dejodasen in het regelen van de embryonale TH niveaus, voor het eerst klaar en duidelijk aantonen dat THs essentieel zijn voor de normale embryonale ontwikkeling bij embryo’s van beenvissen. Female fish deposit a considerable amount of thyroid hormones (THs) into the yolk of their eggs. This large yolk reserve is assumed to be utilized by the developing embryo prior to the onset of its thyroid gland activity. However, it has not been established how important these maternally deposited THs really are, and which role they play during fish embryonic development. We therefore used a multi dimensional approach in an attempt to answer this question, using zebrafish as a model organism. First, we enhanced the thyroid status of zebrafish embryos using a continuous T3 treatment via the rearing medium. This T3 supplementation caused acceleration in embryonic development, hatching and pigmentation, suggestive of a stimulatory role of THs in embryonic development. The changes in development were accompanied by an up regulation of TRα and a down regulation of D2 transcript levels in the T3 treated embryos, indicating that fish embryos can regulate the availability of TH by adjusting deiodinases and the ultimate activity of TH by adjusting TR levels. Next, in an attempt to use parental hypothyroidism to reduce TH deposition into fish eggs and to determine its effect on subsequent embryonic development, adult zebrafish were treated with the goitrogen PTUrea for 8 weeks. However, the treated fish gradually stopped laying eggs, showing that a long term goitrogen treatment clearly affects reproduction. As a result only a small amount of embryos could be collected. In these embryos the embryonic mRNA expression of deiodinases and TRs were not affected, possibly because the embryonic thyroid status was not or not severely affected. Morpholino knock-down of D1 and D2 was the last approach used, with the aim of understanding the influence of minimizing intracellular TH activation on zebrafish embryonic development. Knock-down of D2, but not of D1, clearly delayed several developmental parameters, revealing that the embryonic development of zebrafish is indeed dependent on intracellular TH activation and this process is mainly controlled by D2. The role of D1 in this regard seems to be minor and may only become important when D2 activity is inhibited. Combined knock-down of both D1 and D2 resulted in severe developmental defects and abnormalities, further proving that the complete blocking ORD activity is detrimental for the developing embryo. A significant down regulation of TRβ transcript levels in D2 knock-down embryos together with the ability of T3, but not T4, to rescue the developmental defects, were clear indications that the observed effects resulted from local T3 deprivation in the embryo. The partial cDNA cloning of zebrafish D3 and the subsequent ontogenic expression study revealed that the TH inactivating enzyme D3 is expressed from the beginning of embryonic development and is highly responsive to T3 supplementation. Taken together the accelerated development when TH status is enhanced and the delayed development when THs are deprived, as well as the active role of deiodinases in regulating embryonic TH levels, these data provide the first clear evidence that THs are essential for the normal embryonic development of teleost embryos. parameters, revealing that the embryonic development of zebrafish is indeed dependent on intracellular TH activation and this process is mainly controlled by D2. The role of D1 in this regard seems to be minor and may only become important when D2 activity is inhibited. Combined knock-down of both D1 and D2 resulted in severe developmental defects and abnormalities, further proving that the complete blocking ORD activity is detrimental for the developing embryo. A significant down regulation of TRβ transcript levels in D2 knock-down embryos together with the ability of T3, but not T4, to rescue the developmental defects, were clear indications that the observed effects resulted from local T3 deprivation in the embryo. The partial cDNA cloning of zebrafish D3 and the subsequent ontogenic expression study revealed that the TH inactivating enzyme D3 is expressed from the beginning of embryonic development and is highly responsive to T3 supplementation. Taken together the accelerated development when TH status is enhanced and the delayed development when THs are deprived, as well as the active role of deiodinases in regulating embryonic TH levels, these data provide the first clear evidence that THs are essential for the normal embryonic development of teleost embryos.
Academic collection --- 597.554.3 --- 591.3 --- 577.175.4 --- 591.3 Animal embryology. Animal ontogeny. Development of the individual organism --- Animal embryology. Animal ontogeny. Development of the individual organism --- 597.554.3 Cyprinidae. Carp. Goldfish. Crucian. Tench. Barbel. Bleak. Chub. Dace. Gudgeon. Bitterling. Rudd. Roach. Bream. Loach. Minnow. Lepomis --- Cyprinidae. Carp. Goldfish. Crucian. Tench. Barbel. Bleak. Chub. Dace. Gudgeon. Bitterling. Rudd. Roach. Bream. Loach. Minnow. Lepomis --- 577.175.4 Thyroid hormones. Parathyroid hormones. Thyroxine. Calcitonin --- Thyroid hormones. Parathyroid hormones. Thyroxine. Calcitonin --- Theses
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Immunology. Immunopathology --- Pathological endocrinology --- Clinical chemistry --- Hormones --- Radioimmunoassay --- Radioimmunodosage --- analysis --- Analysis --- Analyse --- Radioimmunoassay. --- -Radioimmunoassay --- Immunoassay --- Immunodiagnosis --- Radioligand assay --- Catecholamines --- Endocrine glands --- Endocrinology --- Secretion --- Radioimmunoassays --- analysis. --- Digestive System. --- Hormones. --- Hormones - Analysis --- Hormones - analysis --- Digestive System --- Cyclic amp --- Cyclic gmp --- Growth --- Hypothalamus --- Methods --- Parathyroid hormones --- Pineal hormones --- Pituitary hormones --- Prostaglandins --- Renal hormones --- Sex --- Steroid hormones --- Thyroid hormones --- Vasoactive peptide hormones
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Bones --- Calcitonin --- Calcium --- Calcium regulating hormones --- Bone Diseases, Metabolic --- Parathyroid Hormones --- Vitamin D --- Diseases --- Etiology --- Congresses. --- Physiological effect --- Therapeutic use --- Metabolism --- Disorders --- Physiology --- Calcium. Metabolisme. Stoornissen. (Congres) --- Thyrocalcitonin / in de therapie. (Congres) --- Beenderen. Ziekten. Oorzaken. (Congres) --- Thyrocalcitonine. Effets physiologiques. (Congrès) --- Calcium. Métabolisme. Troubles. (Congrès) --- Os. Maladies. Causes. (Congrès) --- Thyrocalcitonine / en thérapeutique. (Congrès) --- Thyrocalcitonin. Fysiologisch effect. (Congres)
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