PTH-085 Monoclonal Antibody Therapy in Crohn’S Disease: Does Serial Faecal Calprotectin Play a Role?: Abstract PTH-085 Table 1
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PTH(1-84)/PTH(7-84): a balance of power.
This review considers many new basic and clinical aspects of parathyroid hormone (PTH). We focus especially on the identification of PTH fragments and how they may relate to renal failure, diagnosis, and treatment of secondary hyperparathyroidism and renal osteodystrophy. The biosynthesis and metabolism of PTH, measurement of circulating forms of PTH, the effects of PTH on receptor activation a...
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The purpose of the WAND demonstrator performance measurements was to evaluate how well the requirements of the WAND system design are met. This deliverable sums up the results of the performance evaluation. A special focus is put on evaluation of the WAND specific components that were designed and implemented within the project. The performance of the WAND radio sub-system, consisting of WAND r...
متن کاملCritical role of parathyroid hormone (PTH) receptor-1 phosphorylation in regulating acute responses to PTH.
Agonist-induced phosphorylation of the parathyroid hormone (PTH) receptor 1 (PTHR1) regulates receptor signaling in vitro, but the role of this phosphorylation in vivo is uncertain. We investigated this role by injecting "knock-in" mice expressing a phosphorylation-deficient (PD) PTHR1 with PTH ligands and assessing acute biologic responses. Following injection with PTH (1-34), or with a unique...
متن کاملParathyroid hormone (PTH)-related protein(1-36) is equipotent to PTH(1-34) in humans.
Humoral hypercalcemia of malignancy (HHM) results from the production of PTH-related protein (PTHrP) by human tumors. One previous study has reported the results of human (h) PTHrP(1-34) infusion into humans. In that report, hPTHrP(1-34) was found to be qualitatively similar to but 3- to 10-fold less potent than hPTH(1-34). Because hPTHrP(1-36) and not hPTH(1-34) is likely to be the actual amin...
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BACKGROUND Hyperparathyroidism in humans and continuous parathyroid hormone (cPTH) treatment in mice cause bone loss by regulating the production of RANKL and OPG by stromal cells (SCs) and osteoblasts (OBs). Recently, it has been reported that T cells are required for cPTH to induce bone loss as the binding of the T cell costimulatory molecule CD40L to SC receptor CD40 augments SC sensitivity ...
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ژورنال
عنوان ژورنال: Gut
سال: 2013
ISSN: 0017-5749,1468-3288
DOI: 10.1136/gutjnl-2013-304907.572