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Regulation of parath[y]roid hormone-related protein in adult T-cell leukemia/lymphoma in a severe combined immuno-deficient/beige mouse model of humoral hypercalcemia of malignancyRichard, Virgile B. January 2003 (has links)
Thesis (Ph. D.)--Ohio State University, 2003. / Document formatted into pages; contains xiv, 244 p. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Dec. 3.
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Part I. A study of mechanisms contributing to hypocalcemia in acute pancreatitis. Part II. Variables in the measurement of serum ionized calcium /Marenberg, Stanford P. January 1976 (has links)
No description available.
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Investigations on the pathogenesis of hypercalcemia and malignancy in dogs.Meuten, Donald John January 1981 (has links)
No description available.
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Investigations on the pathogenesis and treatment of humoral hypercalcemia of malignancy using a canine hypercalcemic adenocarcinoma propagated in nude mice /Rosol, Thomas John January 1986 (has links)
No description available.
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Nephrogenous cyclic adenosine monophosphate in primary hepatocellular carcinoma.January 1990 (has links)
by Kam-Ming Au. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1990. / Bibliography: leaves 87-101. / LIST OF TABLES / LIST OF FIGURES / ACKNOWLEDGEMENTS / ABSTRACT / Chapter CHAPTER 1. --- INTRODUCTION --- p.1 / Chapter 1.1 --- Normal calcium homeostasis --- p.1 / Chapter 1.2 --- The incidence and common causes of hypercalcemia in hospital population --- p.6 / Chapter 1.3 --- Hypercalcemia in primary hyperparathyroidism --- p.10 / Chapter 1.4 --- Hypercalcemia of malignancy --- p.13 / Chapter 1.5 --- Pathophysiology of humoral hypercalcemia of malignancy --- p.16 / Chapter 1.6 --- Pathogenesis of humoral hypercalcemia of malignancy-evidence for a parathyroid hormone-related peptide --- p.20 / Chapter 1.7 --- Hypercalcemia in primary hepatocellular carcinoma --- p.27 / Chapter 1.8 --- Physiological role of cyclic adenosine monophosphate --- p.28 / Chapter 1.9 --- Aim of the present study --- p.29 / Chapter CHAPTER 2. --- MATERIALS AND METHODS --- p.30 / Chapter 2.1 --- Patients --- p.30 / Chapter 2.1.1 --- Hepatocellular carcinoma patients --- p.30 / Chapter 2.1.2 --- Cirrhotic patients --- p.30 / Chapter 2.2 --- Healthy control subjects --- p.30 / Chapter 2.3 --- Collection of blood and urine specimens --- p.32 / Chapter 2.4 --- Methods --- p.32 / Chapter 2.4.1 --- Routine chemistries --- p.32 / Chapter 2.4.2 --- Plasma and urine cyclic adenosine monophosphate --- p.33 / Chapter - --- commercial urine controls --- p.34 / Chapter - --- scintillation cocktail --- p.34 / Chapter - --- imprecision study --- p.34 / Chapter - --- accuracy study --- p.34 / Chapter 2.4.3 --- Nephrogenous cyclic adenosine monophosphate and total urinary cyclic adenosine monophosphate / 100 ml glomerular filtrate --- p.35 / Chapter 2.4.4 --- Total urinary cyclic adenosine monophosphate : creatinine ratio --- p.36 / Chapter 2.4.5 --- Components of hypercalcemia --- p.36 / Chapter 2.4.6 --- Urinary hydroxyproline : creatinine ratio --- p.37 / Chapter 2.4.7 --- Renal phosphate threshold --- p.37 / Chapter 2.4.8 --- Serum parathyroid hormone --- p.38 / Chapter 2.4.9 --- Serum parathyroid hormone-related peptide --- p.38 / Chapter 2.5 --- Statistical analysis --- p.39 / Chapter CHAPTER 3. --- RESULTS --- p.40 / Chapter 3.1 --- Method validation for cyclic adenosine monophosphate assay --- p.40 / Chapter 3.1.1 --- Standard curve of the cyclic adenosine monophosphate assay --- p.40 / Chapter 3.1.2 --- Results of imprecision study --- p.43 / Chapter 3.1.3 --- Results of accuracy study --- p.43 / Chapter 3.2 --- "Results of hypercalcemic and normocalcemic hepatocellular carcinoma patients, cirrhotic patients, and healthy control subjects" --- p.47 / Chapter 3.2.1 --- "Results of serum calcium, albumin adjusted calcium, serum albumin and serum alkaline phosphatase" --- p.47 / Chapter 3.2.2 --- "Results of serum phosphate, renal phosphate threshold and serum parathyroid hormone" --- p.51 / Chapter 3.2.3 --- Results of plasma cyclic adenosine monophosphate --- p.55 / Chapter 3.2.4 --- "Results of nephrogenous cyclic adenosine monophosphate , total urinary cyclic adenosine monophosphate / 100 ml glomerular filtrate and total urinary cyclic adenosine monophosphate : creatinine ratio 59" / Chapter 3.2.5 --- Results of urinary calcium : creatinine ratio and urinary hydroxyproline : creatinine ratio --- p.66 / Chapter 3.2.6 --- Factors contributing to hypercalcemia in hepatocellular carcinoma patients 71 / Chapter 3.2.7 --- Results of serum parathyroid hormone-related peptide --- p.75 / Chapter CHAPTER 4. --- DISCUSSION --- p.77 / REFERENCES --- p.87
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Effects of calcium and calciotropic hormones on salivary gland functionSagulin, Gun-Britt. January 1989 (has links)
Thesis (doctoral)--Karolinska Institutet, Stockholm, 1989. / Extra t.p. with thesis statement inserted. Includes bibliographical references.
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Effects of calcium and calciotropic hormones on salivary gland functionSagulin, Gun-Britt. January 1989 (has links)
Thesis (doctoral)--Karolinska Institutet, Stockholm, 1989. / Extra t.p. with thesis statement inserted. Includes bibliographical references.
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Etude des causes génétiques de dérégulation du métabolisme de la vitamine D / Study of genetic causes of vitamin D metabolism dysregulationMolin, Arnaud 09 October 2019 (has links)
La vitamine D (D3 ou cholécalciférol du règne animal et D2 ou ergostérol du règne végétal) est une hormone pléiotrope qui possède de nombreux effets biologiques incluant la régulation du métabolisme du calcium et du phosphate. Chez l’Homme, ce composé est synthétisé au niveau cutané sous forme inactive. On décrit ainsi le métabolisme de la vitamine D qui conduit à la production de métabolites actifs (par les vitamine D 25- et 1α-hydroxylases codées par les gènes CYP2R1 et CYP27B1) et à leur dégradation par la vitamine D 24-hydroxylase (gène CYP24A1). L’expression des vitamine 1α- et 24-hydroxylases est finement et inversement régulée afin de maintenir l’homéostasie phosphocalcique, grâce à plusieurs boucles de rétrocontrôle impliquant entre autres la forme 1,25-dihydroxylée de la vitamine D et son récepteur VDR, la calcémie et la parathormone, la phosphatémie et le FGF23. La carence en vitamine D et les défauts de son activation sont associés à un phénotype de rachitisme, tandis que les excès en vitamine D sont associés à un phénotype d’hypercalcémie-hypercalciurie par intoxication (surdosage) ou hypersensibilité à la vitamine D (excès d’activation ou défaut de dégradation).L’objectif de ce travail de thèse est d’identifier des causes génétiques de dérégulation du métabolisme de la vitamine D et de préciser leurs mécanismes physiopathologiques par une description précise du phénotype associé. Pour ce faire, nous avons utilisé de façon conjointe les outils de la génétique (séquençage nouvelle génération et Sanger) et de la biochimie (dosage des métabolites) dans une cohorte de patients recrutés grâce au centre de référence maladies rares du métabolisme du calcium et du phosphate.Ce travail a permis de préciser le rôle de deux gènes dans les maladies liées à la dérégulation métabolisme de la vitamine D, CYP2R1 et CYP24A1, par la mise en évidence de mutations perte de fonction chez des patients avec un phénotype de rachitisme à 25-hydroxyvitamine D basse et d’hypersensibilité à la vitamine D respectivement. Notre étude a permis aussi de préciser le phénotype de ces affections. Dans la cohorte des patients étudiés, l’identification de mutations de gènes impactant le métabolisme du phosphate (SLC34A1 et SLC34A3), souligne l’intérêt de l’étude des facteurs régulateurs des activités vitamine D 1α- et 24-hydroxylases.Aucune variation significative dans les régions promotrices proximales de CYP27B1 et CYP24A1 n’a été identifiée. Le peu de connaissances sur l’ensemble des éléments régulateurs chez l’Homme n’a pas permis d’approfondir notre étude. L’identification et l’étude de ces éléments régulateurs distaux permettra de déterminer leur implication dans les maladies rares du métabolisme de la vitamine D. / The vitamin D (D3 or cholecalciferol from animal kingdom and D2 or ergosterol from plan kingdom) is a pleiotropic hormone who has numerous biological effects including the regulation of calcium and phosphate metabolism. In humans, this compound is synthetized in skin in an inactive form. Thus, we call vitamin D metabolism the biological process which leads to the production of active metabolites (by enzymes 25- and 1α-hydroxylases encoded by CYP2R1 and CYP27B1 genes) and its degradation by vitamin D 24-hydroxylase (gene CYP24A1). The expression of 1α- and 24-hydroxylases is tightly and inversely regulated to maintain calcium and phosphate homeostasis, thanks to several feedback loops including 1,25-dihydroxyvitamin D and its receptor VDR, serum calcium and parathormone, serum phosphate and FGF23. Vitamin D deficiency and vitamin D activation deficiency are associated with rickets, while vitamin D excess are associated with hypercalcemia-hypercalciuria due to vitamin D intoxication (overdose) or hypersensitivity to vitamin D (activation excess or degradation deficiency).Our aim is to identify genetic causes of vitamin D metabolism deregulation and to specify pathophysiologic mechanisms describing phenotype. Thus, we jointly used the tools of genetics (next-generation and Sanger sequencing) and biochemistry (vitamin D metabolites assay) in a cohort of human patients ascertained thanks to the national center for rare diseases of calcium and phosphate metabolism.This work allowed us to specify the role of two genes in diseases of vitamin D metabolism, CYP2R1 and CYP24A1, showing loss of function mutations in patients with rickets and low 25-hydroxyvitamin D and hypersensitivity to vitamin D, respectively. Our study brought new phenotypic elements in these affections. In our cohort of patients, the identification of mutations leading to phosphate deregulation (in SLC34A1 and SLC34A3) highlights the putative role of regulators of vitamin D 1α- and 24-hydroxylases activities in pathophysiology.No significant variation have been identified in the proximal promoting regions of CYP27B1 and CYP24A1. We could not go further considering the lack of knowledge in regulating regions and factors in humans. Identifying distal regulators will allow to study their implication in rare diseases of vitamin D metabolism.
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Frequency and determinants of serum calcium monitoring during eldecalcitol therapy in patients with osteoporosis / 骨粗鬆症患者におけるエルデカルシトール治療中の血清カルシウム検査の実施頻度および関連因子Ri, Kairi 25 March 2024 (has links)
京都大学 / 新制・課程博士 / 博士(医学) / 甲第25185号 / 医博第5071号 / 京都大学大学院医学研究科医学専攻 / (主査)教授 山本 洋介, 教授 寺田 智祐, 教授 柳田 素子 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM
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Molecular and clinical genetic studies of a novel variant of familial hypercalcemia /Szabo, Eva. January 2002 (has links)
Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 4 uppsatser.
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