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Conductive Polymers Derived Heteroatom Doped Carbon Catalysts forOxygen Reduction ReactionHonorato, Ana Maria Borges 22 January 2021 (has links)
No description available.
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A Mathematical Model of Acute Response of Parathyroid Hormone to Changes in Plasma Ionized Calcium in Normal HumansShrestha, Rajiv P 01 January 2008 (has links) (PDF)
A complex bio-mechanism, referred to as calcium homeostasis, regulates plasma ionized calcium (Ca++) concentration in the human body to within a narrow physiologic range which is crucial for maintaining normal physiology and metabolism. Various metabolic disorders and pathologic conditions originate from acute and/or chronic disturbances/disorders in calcium homeostatic system. This system relies on numerous sub-systems which operate in different time-scales ranging from minutes to weeks. In this thesis we focus on a particular sub-system that operates on the time-scale of minutes; the dynamics involves the response of the parathyroid glands to acute changes in plasma Ca++ concentration. We develop a two-pool, linear time-varying model describing the dynamics of the sub-system. We show that this model can predict dynamics observed in clinical tests of induced hypo- and hyper-calcemia in normal humans. In addition, we develop a new protocol for the construction of a Ca-PTH reverse sigmoid curve based on the mathematical model. This protocol removes deficiencies in current protocols in that the resulting curve is invariant with respect to the subject's axis dynamics and calcium clamp test dynamics.
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Calcium/Phosphate Regulation: A Control Engineering ApproachChristie, Christopher Robert 10 January 2014 (has links)
Calcium (Ca) homeostasis is the maintenance of a stable plasma Ca concentration in the human body in the presence of Ca variability in the physiological environment (e.g. by ingestion and/or excretion). For normal physiological function, the total plasma Ca concentration must be maintained within a very narrow range (2.2-2.4mM). Meeting such stringent requirements is the task of a regulatory system that employs parathyroid hormone (PTH) and calcitriol (CTL) to regulate Ca flux between the plasma and the kidneys, intestines and bones. On the other hand, plasma phosphate control is less tightly, but simultaneously, regulated via the same hormonal actions. Chronic imbalances in plasma Ca levels are associated with disorders of the regulatory organs, which cause abnormal hormonal secretion and activity. These changes in hormonal activity may lead to long-term problems, such as, osteoporosis (increased loss of bone mineral density), which arises from primary hyperparathyroidism (PHPT) – hyper secretion of PTH.
Existing in silico models of Ca homeostasis in humans are often cast in the form of a single monolithic system of differential equations and are not easily amenable to the sort of tractable quantitative analysis from which one can acquire useful fundamental insight. In this research, the regulatory systems of plasma Ca and plasma phosphate are represented as an engineering control system where the physiological sub-processes are mapped onto corresponding block components (sensor, controller, actuator and process) and underlying mechanisms are represented by differential equations. Following validation of the overall model, Ca-related pathologies are successfully simulated through induced defects in the control system components.
A systematic approach is used to differentiate PHPT from other diseases with similar pathophysiologies based on the unique hormone/ion responses to short-term Ca disturbance in each pathology model. Additionally, based on the changes in intrinsic parameters associated with PTG behavior, the extent of PHPT progression can be predicted and the enlarged gland size estimated a priori.
Finally, process systems engineering methods are used to explore therapeutic intervention in two Ca-related pathologies: Primary (PHPT) and Secondary (SHPT) Hyperparathyroidism. Through parametric sensitivity analysis and parameter space exploration, the calcium-sensing receptor (sensor) is identified as a target site in both diseases and the extent of potential improvement is determined across the spectrum of severity of PHPT. The findings are validated against existing drug therapy, leading to a method of predicting drug dosage for a given stage of PHPT. Model Predictive Control is used in drug therapy in SHPT to customize the drug dosage for individual patients given the desired PTH outcome, and drug administration constraints. / Ph. D.
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Rôle de la voie de signalisation Gαq/11 dans la réponse osseuse à la parathormone : étude chez un modèle murin insuffisant rénal chronique avec inactivation osseuse de la voie de signalisation Gαq/11 / Role of the Gαq/11 intracellular pathway in the parathyroid hormone bone action : study in a bone specific Gαq/11 deficient mice with chronic renal failureZaloszyc, Ariane 10 October 2018 (has links)
La parathormone joue un rôle clé dans l’homéostasie osseuse. En se liant à l’ostéoblaste par son récepteur, elle active la voie de signalisation Gαs/PKA qui a un rôle ostéoanabolique, et la voie Gα q/11/PKC, dont le rôle n’est que partiellement connu. Lors de l’insuffisance rénale chronique, les patients présentent une hyperparathyroïdie (HPT) et des atteintes osseuses. Notre objectif était de décrire le rôle osseux de la voie PKC dans un modèle de souris transgéniques (Tg) inactivées pour Gα q/11/PKC au niveau osseux, avec ou sans HPT induite par un régime enrichi en phosphate et/ou une insuffisance rénale. Nous avons développé une méthode de quantification scintigraphique osseuse in vivo pour le suivi longitudinal ostéoblastique, et étudié les modifications biochimiques et structurales par µCT. Les souris Tg, comparées aux contrôles, avaient une activité ostéoblastique augmentée et des altérations de la structure osseuse. En cas d’insuffisance rénale, les altérations osseuses et l’activité ostéoblastique étaient moins importantes. L’inactivation de la voie PKC avait donc un rôle osseux protecteur lors de l’HPT modérée de l’insuffisance rénale. / Parathyroid hormone (PTH) plays a crucial role in bone homeostasis. PTH binds to its receptor in osteoblasts and activates two distinct pathways, the Gαs/PKA and the Gαq/11/PKC pathway. Whereas Gαs/PKA has osteoanabolic action, the role of the latter is uncertain. Chronic kidney disease (CKD) leads to hyperparathyroidism and osteodystrophy. This study explores the role of Gα q/11/PKC signaling in osteoblast specific Gα q/11/PKC knockout (Ko) mice under physiological conditions and in hyperparathyroidism induced by high phosphate diet and/or CKD. To this end a quantitative bone planar scintigraphic method was established, allowing for in vivo follow up study of osteoblast activity and related to µCT and biochemical findings. Gα q/11/PKC Ko mice have increased osteoblast activity and bone microarchitectural impairment. CKD Ko mice exhibit a decreased osteoblast activity and preserved bone architecture compared to control. Thus, PKC inactivation may protect bone in case of moderate hyperparathyroidism secondary to CKD.
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FGF23 - a possible PhosphatoninMarsell, Richard January 2008 (has links)
<p>Human physiology is dependent on an accurate phosphate (Pi) homeostasis. Defective Pi regulation causes hyper- or hypophosphatemia, which are associated with ectopic calcification or impaired bone mineralization, and a shortened life span. Current endocrine models of Pi homeostasis are incomplete. However, studies of acquired and hereditary disorders of Pi homeostasis have revealed new potential Pi regulating hormones, Phosphatonin(s). One of these is fibroblast growth factor-23 (FGF23). FGF23 is produced in bone and is secreted into the circulation. Mutations in FGF23 causes disturbed Pi regulation, without the appropriate counter-regulatory actions of parathyroid hormone or vitamin D. By the generation of FGF23 transgenic mice, which display phenotypic similarities to patients with hypophosphatemic disorders, we show that FGF23 exerts endocrine actions in the kidney and causes osteomalacia. Renal FGF23 actions severely decrease Pi reabsorption and expression of Klotho, a suggested age suppressor gene, known to be crucial in FGF23 receptor binding and activation. In bone, our transgenic model displays impaired osteoclast polarization, which should be detrimental to osteoclastic bone resorption in osteomalacia. However, in our model osteoclasts efficiently participate in bone matrix degradation. Furthermore, we investigated a large population-based cohort in order to elucidate the role of FGF23 in normal physiology. Importantly, we were able to demonstrate an association of FGF23 to parathyroid hormone, renal function and bone mineral density and we found a correlation of FGF23 to weight and body fat mass. The studies on which this thesis is based, demonstrate that FGF23 has phosphatonin-like properties and that the skeleton functions as an endocrine organ. In addition, the results indicate that FGF23 has a role in bone mineral and lipid metabolism, and that FGF23 is a possible diagnostic marker and therapeutic target for the future.</p>
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Avaliação da concentração sérica de paratormônio intacto em gatos com doença renal crônica / Intact serum parathyroid hormone evaluation in cats with chronic kidney diseaseGiovaninni, Luciano Henrique 30 September 2010 (has links)
A doença renal crônica (DRC) evolui de forma progressiva e o hiperparatiroidismo secundário renal (HPTSR) é uma das importantes alterações que causa a perda adicional de néfrons e o comprometimento de varios sistemas; o paratormônio (PTH) é considerado como uma importante toxina urêmica. A avaliação do PTH sérico em felinos com DRC pode trazer informações para o melhor entendimento da fisiopatologia do HPTSR, suscitando possíveis medidas terapêuticas. Observou-se que gatos com DRC (n=40) apresentaram aumento significante (p < 0,05) da concentração sérica de paratormônio intacto (PTHi) quando comparados a gatos clinicamente normais (n=21; grupo controle). Quanto a avaliação do PTHi nos subgrupos de DRC (ESTÁGIOS II, III e IV de evolução da afecção, classificados segundo o International Renal Interest Society IRIS), constatou-se diferença significante entre os gatos dos ESTÁGIOS III e IV com os gatos clinicamente normais; em relação ao ESTÁGIO II, apesar de não ter sido observada diferença significante, a maioria dos gatos apresentou aumento da concentração sérica de PTHi (> 60,2 pg/mL). Em relação aos valores das concentrações séricas de fósforo e de cálcio iônico, detectou-se a tendência de concentrações séricas progressivamente maiores de fósforo (hiperfosfatemia) nos estágios mais avançados da doença (frequências de 16,7%, 27,3% e 100% nos ESTÁGIOS II, III e IV, respectivamente); inversamente, as concentrações séricas de cálcio iônico foram progressivamente menores (respectivamente, frequência de hipocalcemia de 8,3%, 9,1% e 66,7%). Constatou-se diferença significante quanto as concentração de bicarbonato plasmático entre os gatos clinicamente normais e os gatos com DRC (acidose metabólica em 42,5% dos casos), como também entre os gatos clinicamente normais e os animais dos subgrupos DRC ESTÁGIOS II e III (bicarbonato plasmático < 16,8 mmol/L observado em 40,9% e 33,3%, respectivamente). Não foram detectadas diferenças significantes quanto as concentrações séricas de cálcio total ou de pH sanguíneo nas comparações múltiplas. Em relação aos valores da multiplicação entre as concentrações séricas de cálcio total e de fósforo, a análise estatística demonstrou resultados similares àqueles da análise das concentrações séricas de fósforo. Sugere-se que o estímulo para o aumento da concentração sérica de PTHi, e o consequente HPTSR, observado nos gatos com DRC no estágio IV, tenha decorrido da hipocalcemia iônica e da hiperfosfatemia apresentadas por estes animais, ativando a regulação pela paratireóide. Quanto aos gatos nos estágios II e III da DRC, outros fatores, além da hipocalcemia e da hiperfosfatemia, devem estar envolvidos no aumento da síntese de PTHi, sugerindo-se a necessidade de investigação, por exemplo, das concentrações séricas de calcitriol; ainda no subgrupo ESTÁGIO II, a hipercalcemia iônica observada em 50% dos gatos sugere a possibilidade do envolvimento da acidose metabólica, que poderia comprometer a fração ionizada do cálcio. A correlação positiva observada entre o fósforo e o PTHi sugere a possibilidade de avaliação indireta de HPTSR pela determinação do fósforo sérico; entretanto nos gatos nos estágios II e III da DRC, esta avaliação indireta não se mostrou adequada, pois observou-se concomitantemente normofosfatemia e aumento do PTHi, indicando-se a necessidade da determinação do PTHi para avaliação do HPTSR nesses estágios da DRC em gatos. / Chronic kidney disease (CKD) develops gradually, causing several changes and renal secondary hyperparathyroidism (RSHPTH) is one of those alterations, which, besides causing loss of additional nephrons, increases the morbidity and mortality due to the action of parathyroid hormone (PTH) as an important uremic toxin. Evaluation of serum PTH in cats with CKD may add information for the better understanding of RSHPTH pathophysiology, arising possible therapeutic procedures. Cats with CKD (n = 40) showed significant increase (p < 0.05) in serum intact parathyroid hormone (iPTH) as compared with clinically normal cats (n = 21, control group). In subgroups of CKD (STAGES II, III and IV of CKD, classified as recommended by International Renal Interest Society - IRIS), significant difference was observed between clinically normal cats and cats with CKD in STAGES III and IV; in reference to the STAGE II, although no significant difference was observed, most of these cats showed an increase in serum iPTH (> 60.2 pg / mL). In relation to values of phosphorus and ionized calcium serum concentrations, a trend of progressively higher serum concentrations of phosphorus (hyperphosphatemia) was detected in the late stages of the disease (16.7%, 27.3% and 100% in STAGES II, III and IV, respectively), in opposite, serum concentrations of ionized calcium progressively decreased (respectively, ionized hypocalcemia, 8.3%, 9.1% and 66.7%). Plasma bicarbonate concentrations were significant different between clinically normal cats and cats with CKD (metabolic acidosis observed in 42.5% of the cases), and between clinically normal cats and cats with CKD STAGES II and III (plasma bicarbonate < 16.8 mmol/L observed in 40.9% and 33.3% of the cases, respectively). No significant differences were detected for serum concentrations of total calcium and blood pH, in multiple comparisons analysis. In relation to the values of serum concentrations of calcium and phosphorus product, the results were similar to those obtained from phosphorus serum concentrations evaluation. The results suggested that the stimulus for the increase in serum iPTH, and follow development of RSHPTH, observed in cats with CKD STAGE IV, was in consequence of ionized hypocalcemia and hyperphosphatemia, enabling the regulation by the parathyroid. However, for the cats in STAGES II and III of CKD, other factors, beyond hypocalcemia and hyperphosphatemia, may be involved to cause the increase of iPTH synthesis, and calcitriol serum concentrations must be investigated; in cats with DRC STAGE II, 50% of the cases presented ionized hypercalcemia, suggesting the influence of metabolic acidosis in ionized calcium fraction. The correlation observed between serum phosphorus and iPTH may suggest the possibility of indirect evaluation of RSHPTH by means of phosphorus serum concentration; however in cats with DRC, STAGES II and III, this indirect assessment may not be adequate as normal serum levels of phosphorus as well as increased serum iPTH were observed in those cats, indicating the need for the determination of serum iPTH to evaluate RSHPTH.
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FGF23 - a possible PhosphatoninMarsell, Richard January 2008 (has links)
Human physiology is dependent on an accurate phosphate (Pi) homeostasis. Defective Pi regulation causes hyper- or hypophosphatemia, which are associated with ectopic calcification or impaired bone mineralization, and a shortened life span. Current endocrine models of Pi homeostasis are incomplete. However, studies of acquired and hereditary disorders of Pi homeostasis have revealed new potential Pi regulating hormones, Phosphatonin(s). One of these is fibroblast growth factor-23 (FGF23). FGF23 is produced in bone and is secreted into the circulation. Mutations in FGF23 causes disturbed Pi regulation, without the appropriate counter-regulatory actions of parathyroid hormone or vitamin D. By the generation of FGF23 transgenic mice, which display phenotypic similarities to patients with hypophosphatemic disorders, we show that FGF23 exerts endocrine actions in the kidney and causes osteomalacia. Renal FGF23 actions severely decrease Pi reabsorption and expression of Klotho, a suggested age suppressor gene, known to be crucial in FGF23 receptor binding and activation. In bone, our transgenic model displays impaired osteoclast polarization, which should be detrimental to osteoclastic bone resorption in osteomalacia. However, in our model osteoclasts efficiently participate in bone matrix degradation. Furthermore, we investigated a large population-based cohort in order to elucidate the role of FGF23 in normal physiology. Importantly, we were able to demonstrate an association of FGF23 to parathyroid hormone, renal function and bone mineral density and we found a correlation of FGF23 to weight and body fat mass. The studies on which this thesis is based, demonstrate that FGF23 has phosphatonin-like properties and that the skeleton functions as an endocrine organ. In addition, the results indicate that FGF23 has a role in bone mineral and lipid metabolism, and that FGF23 is a possible diagnostic marker and therapeutic target for the future.
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Avaliação da concentração sérica de paratormônio intacto em gatos com doença renal crônica / Intact serum parathyroid hormone evaluation in cats with chronic kidney diseaseLuciano Henrique Giovaninni 30 September 2010 (has links)
A doença renal crônica (DRC) evolui de forma progressiva e o hiperparatiroidismo secundário renal (HPTSR) é uma das importantes alterações que causa a perda adicional de néfrons e o comprometimento de varios sistemas; o paratormônio (PTH) é considerado como uma importante toxina urêmica. A avaliação do PTH sérico em felinos com DRC pode trazer informações para o melhor entendimento da fisiopatologia do HPTSR, suscitando possíveis medidas terapêuticas. Observou-se que gatos com DRC (n=40) apresentaram aumento significante (p < 0,05) da concentração sérica de paratormônio intacto (PTHi) quando comparados a gatos clinicamente normais (n=21; grupo controle). Quanto a avaliação do PTHi nos subgrupos de DRC (ESTÁGIOS II, III e IV de evolução da afecção, classificados segundo o International Renal Interest Society IRIS), constatou-se diferença significante entre os gatos dos ESTÁGIOS III e IV com os gatos clinicamente normais; em relação ao ESTÁGIO II, apesar de não ter sido observada diferença significante, a maioria dos gatos apresentou aumento da concentração sérica de PTHi (> 60,2 pg/mL). Em relação aos valores das concentrações séricas de fósforo e de cálcio iônico, detectou-se a tendência de concentrações séricas progressivamente maiores de fósforo (hiperfosfatemia) nos estágios mais avançados da doença (frequências de 16,7%, 27,3% e 100% nos ESTÁGIOS II, III e IV, respectivamente); inversamente, as concentrações séricas de cálcio iônico foram progressivamente menores (respectivamente, frequência de hipocalcemia de 8,3%, 9,1% e 66,7%). Constatou-se diferença significante quanto as concentração de bicarbonato plasmático entre os gatos clinicamente normais e os gatos com DRC (acidose metabólica em 42,5% dos casos), como também entre os gatos clinicamente normais e os animais dos subgrupos DRC ESTÁGIOS II e III (bicarbonato plasmático < 16,8 mmol/L observado em 40,9% e 33,3%, respectivamente). Não foram detectadas diferenças significantes quanto as concentrações séricas de cálcio total ou de pH sanguíneo nas comparações múltiplas. Em relação aos valores da multiplicação entre as concentrações séricas de cálcio total e de fósforo, a análise estatística demonstrou resultados similares àqueles da análise das concentrações séricas de fósforo. Sugere-se que o estímulo para o aumento da concentração sérica de PTHi, e o consequente HPTSR, observado nos gatos com DRC no estágio IV, tenha decorrido da hipocalcemia iônica e da hiperfosfatemia apresentadas por estes animais, ativando a regulação pela paratireóide. Quanto aos gatos nos estágios II e III da DRC, outros fatores, além da hipocalcemia e da hiperfosfatemia, devem estar envolvidos no aumento da síntese de PTHi, sugerindo-se a necessidade de investigação, por exemplo, das concentrações séricas de calcitriol; ainda no subgrupo ESTÁGIO II, a hipercalcemia iônica observada em 50% dos gatos sugere a possibilidade do envolvimento da acidose metabólica, que poderia comprometer a fração ionizada do cálcio. A correlação positiva observada entre o fósforo e o PTHi sugere a possibilidade de avaliação indireta de HPTSR pela determinação do fósforo sérico; entretanto nos gatos nos estágios II e III da DRC, esta avaliação indireta não se mostrou adequada, pois observou-se concomitantemente normofosfatemia e aumento do PTHi, indicando-se a necessidade da determinação do PTHi para avaliação do HPTSR nesses estágios da DRC em gatos. / Chronic kidney disease (CKD) develops gradually, causing several changes and renal secondary hyperparathyroidism (RSHPTH) is one of those alterations, which, besides causing loss of additional nephrons, increases the morbidity and mortality due to the action of parathyroid hormone (PTH) as an important uremic toxin. Evaluation of serum PTH in cats with CKD may add information for the better understanding of RSHPTH pathophysiology, arising possible therapeutic procedures. Cats with CKD (n = 40) showed significant increase (p < 0.05) in serum intact parathyroid hormone (iPTH) as compared with clinically normal cats (n = 21, control group). In subgroups of CKD (STAGES II, III and IV of CKD, classified as recommended by International Renal Interest Society - IRIS), significant difference was observed between clinically normal cats and cats with CKD in STAGES III and IV; in reference to the STAGE II, although no significant difference was observed, most of these cats showed an increase in serum iPTH (> 60.2 pg / mL). In relation to values of phosphorus and ionized calcium serum concentrations, a trend of progressively higher serum concentrations of phosphorus (hyperphosphatemia) was detected in the late stages of the disease (16.7%, 27.3% and 100% in STAGES II, III and IV, respectively), in opposite, serum concentrations of ionized calcium progressively decreased (respectively, ionized hypocalcemia, 8.3%, 9.1% and 66.7%). Plasma bicarbonate concentrations were significant different between clinically normal cats and cats with CKD (metabolic acidosis observed in 42.5% of the cases), and between clinically normal cats and cats with CKD STAGES II and III (plasma bicarbonate < 16.8 mmol/L observed in 40.9% and 33.3% of the cases, respectively). No significant differences were detected for serum concentrations of total calcium and blood pH, in multiple comparisons analysis. In relation to the values of serum concentrations of calcium and phosphorus product, the results were similar to those obtained from phosphorus serum concentrations evaluation. The results suggested that the stimulus for the increase in serum iPTH, and follow development of RSHPTH, observed in cats with CKD STAGE IV, was in consequence of ionized hypocalcemia and hyperphosphatemia, enabling the regulation by the parathyroid. However, for the cats in STAGES II and III of CKD, other factors, beyond hypocalcemia and hyperphosphatemia, may be involved to cause the increase of iPTH synthesis, and calcitriol serum concentrations must be investigated; in cats with DRC STAGE II, 50% of the cases presented ionized hypercalcemia, suggesting the influence of metabolic acidosis in ionized calcium fraction. The correlation observed between serum phosphorus and iPTH may suggest the possibility of indirect evaluation of RSHPTH by means of phosphorus serum concentration; however in cats with DRC, STAGES II and III, this indirect assessment may not be adequate as normal serum levels of phosphorus as well as increased serum iPTH were observed in those cats, indicating the need for the determination of serum iPTH to evaluate RSHPTH.
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Improving the outcomes of patients with chronic kidney disease-mineral bone disorderEddington, Helen January 2013 (has links)
Chronic Kidney Disease-Mineral Bone Disorder (CKD-MBD) is a systemic disorder which includes abnormal bone chemistry, vascular or soft tissue calcification, and abnormal bone formation. Many of the parameters of CKD-MBD have been associated with an increased mortality risk in renal patients. There were three main facets to this research project. The first aim of this research was to perform two different studies using the Chronic Renal Insufficiency Standards Implementation Study (CRISIS) data. This prospective epidemiological study is designed to identify factors associated with renal progression and survival in the pre-dialysis CKD population. We have shown that for each 0.323mmol/L (1mg/dL) increase in serum phosphate there was a significant stepwise increased risk of death. (HR1.3 (1.1, 1.5) P=0.01). The association of baseline phenotypic data against vascular stiffness measurements was also investigated. Augmentation index measured at the radial artery was associated with a raised systolic blood pressure but no association with biochemical abnormalities was found.We hypothesised that the phosphate effect on survival was related to the effects within the CKD-MBD spectrum and therefore control of secondary hyperparathyroidism would improve bone and cardiovascular parameters. Therefore for the second part of this research we performed a randomised controlled trial to examine the effects of cinacalcet with standard therapy compared to standard therapy alone on bone and cardiovascular parameters in haemodialysis patients with uncontrolled hyperparathyroidism. The change of biochemical parameters and cardiovascular markers were also further explored in secondary analyses alongside survival data. The primary end point of change in vascular calcification at 52 weeks showed no significant difference between arms. As equivalent control of phosphate and iPTH was achieved in both arms secondary analyses were performed. This showed a significant regression of left ventricular hypertrophy and carotid intima-media thickness associated with phosphate but not iPTH reduction. Patients whose phosphate reduced during the study had a survival advantage when followed for 5 years (HR=10.2 (1.1, 104.5) P=0.049). The third part of this research was to investigate iPTH assay variability. We explored the variation in iPTH assays across the North West and paired this with regional audit data. This study showed that despite there being significant variation among iPTH assays across the region the variation in clinical management was still accounting for some variation in achieving PTH targets.In conclusion, serum phosphate, within the normal laboratory range, is associated with an increased mortality in CKD patients. Haemodialysis patients may have improvement of cardiovascular outcomes with tight control of secondary hyperparathyroidism, by whichever therapeutic means. Intact PTH assays variation may alter our clinical management but variation in practice still affects guideline achievement.
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Modulation of the intestinal vitamin D receptor and calcium ATPase activity by essential fatty acid supplementationLeonard, Franciska 04 January 2007 (has links)
Please read the abstract in the front section of this document / Dissertation (MSc (Physiology))--University of Pretoria, 2007. / Physiology / unrestricted
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