The Experts below are selected from a list of 51 Experts worldwide ranked by ideXlab platform
Xiaodong Li - One of the best experts on this subject based on the ideXlab platform.
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Etelcalcetide, A Novel Calcimimetic, Prevents Vascular Calcification in A Rat Model of Renal Insufficiency with Secondary HyperParathyroidism
Calcified Tissue International, 2017Co-Authors: Longchuan Yu, James E. Tomlinson, Shawn T. Alexander, Kelly Hensley, Denise Dwyer, Marina Stolina, Charles Dean, William G. Goodman, William G. Richards, Xiaodong LiAbstract:Etelcalcetide, a novel peptide agonist of the calcium-sensing receptor, prevents vascular calcification in a rat model of renal insufficiency with secondary hyperParathyroidism. Vascular calcification occurs frequently in patients with chronic kidney disease (CKD) and is a consequence of impaired mineral homeostasis and secondary hyperParathyroidism (SHPT). Etelcalcetide substantially lowers Parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF23) levels in SHPT patients on hemodialysis. This study compared the effects of etelcalcetide and paricalcitol on vascular calcification in rats with adenine-induced CKD and SHPT. Uremia and SHPT were induced in male Wistar rats fed a diet supplemented with 0.75% adenine for 4 weeks. Rats were injected with vehicle, etelcalcetide, or paricalcitol for 4 weeks from the beginning of adenine diet. Rats fed an adenine-free diet were included as nonuremic controls. Similar reductions in plasma PTH and Parathyroid Chief Cell proliferation were observed in both etelcalcetide- and paricalcitol-treated rats. Serum calcium and phosphorus were significantly lower in etelcalcetide-treated uremic rats and was unchanged in paricalcitol-treated rats. Both serum FGF23 and aortic calcium content were significantly lower in etelcalcetide-treated uremic rats compared with either vehicle- or paricalcitol-treated uremic rats. The degree of aortic calcium content for etelcalcetide-treated rats was similar to that in nonuremic controls and corroborated findings of lack of histologic aortic mineralization in those groups. In conclusion, etelcalcetide and paricalcitol similarly attenuated progression of SHPT in an adenine rat model of CKD. However, etelcalcetide differentially prevented vascular calcification, at least in part, due to reductions in serum FGF23, calcium, and phosphorus levels.
Longchuan Yu - One of the best experts on this subject based on the ideXlab platform.
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Etelcalcetide, A Novel Calcimimetic, Prevents Vascular Calcification in A Rat Model of Renal Insufficiency with Secondary HyperParathyroidism
Calcified Tissue International, 2017Co-Authors: Longchuan Yu, James E. Tomlinson, Shawn T. Alexander, Kelly Hensley, Denise Dwyer, Marina Stolina, Charles Dean, William G. Goodman, William G. Richards, Xiaodong LiAbstract:Etelcalcetide, a novel peptide agonist of the calcium-sensing receptor, prevents vascular calcification in a rat model of renal insufficiency with secondary hyperParathyroidism. Vascular calcification occurs frequently in patients with chronic kidney disease (CKD) and is a consequence of impaired mineral homeostasis and secondary hyperParathyroidism (SHPT). Etelcalcetide substantially lowers Parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF23) levels in SHPT patients on hemodialysis. This study compared the effects of etelcalcetide and paricalcitol on vascular calcification in rats with adenine-induced CKD and SHPT. Uremia and SHPT were induced in male Wistar rats fed a diet supplemented with 0.75% adenine for 4 weeks. Rats were injected with vehicle, etelcalcetide, or paricalcitol for 4 weeks from the beginning of adenine diet. Rats fed an adenine-free diet were included as nonuremic controls. Similar reductions in plasma PTH and Parathyroid Chief Cell proliferation were observed in both etelcalcetide- and paricalcitol-treated rats. Serum calcium and phosphorus were significantly lower in etelcalcetide-treated uremic rats and was unchanged in paricalcitol-treated rats. Both serum FGF23 and aortic calcium content were significantly lower in etelcalcetide-treated uremic rats compared with either vehicle- or paricalcitol-treated uremic rats. The degree of aortic calcium content for etelcalcetide-treated rats was similar to that in nonuremic controls and corroborated findings of lack of histologic aortic mineralization in those groups. In conclusion, etelcalcetide and paricalcitol similarly attenuated progression of SHPT in an adenine rat model of CKD. However, etelcalcetide differentially prevented vascular calcification, at least in part, due to reductions in serum FGF23, calcium, and phosphorus levels.
Göran Åkerström - One of the best experts on this subject based on the ideXlab platform.
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Surgical Management of Multiglandular Parathyroid Disease
2013Co-Authors: Göran Åkerström, Peter StålbergAbstract:In 1934, Albright et al.[1] discovered the unusual entity of Parathyroid water-clear–Cell hyperplasia and thought this resulted from some form of extrinsic glandular stimulation. The more common Parathyroid Chief-Cell hyperplasia was described in 1958 by Cope et al.[2] and was believed to have a similar genesis. However, stimulating agents causing the disease have still not been identified in sporadic Parathyroid hyperplasia, in contrast to hyperParathyroidism (HPT) secondary to uremia or long-term lithium therapy (see Chapter 66, Surgical Management of Secondary and Tertiary HyperParathyroidism). Despite the fact that they represent a minority among HPT patients, ever since the early days of Parathyroid surgery cases of Parathyroid hyperplasia have continued to intrigue pathologists and Parathyroid surgeons (see Chapter 70, Surgical Pathology of the Parathyroid Glands). Hyperplasia is easily …
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Expression and function of a CD4-like molecule in Parathyroid tissue.
Surgery, 1996Co-Authors: Per Hellman, Göran Åkerström, Jonas Rastad, Alex Karlsson-parra, Lars Klareskog, Peter Ridefelt, Gunnel Bjerneroth, Claes JuhlinAbstract:BACKGROUND: Parathyroid tissue expresses the T-lymphocyte antigens CD3 and CD4, and Parathyroid CD3 has earlier been proposed to interact in the regulation of Parathyroid hormone (PTH) release. METHODS: Anti-Leu3a, a monoclonal antibody recognizing CD4, was used to stain Parathyroid tissue immunohistochemically, to influence PTH secretion from enzymatically dispersed Parathyroid Cells, and to immunoprecipitate Parathyroid CD4. Northern blot and polymerase chain reaction were used to clarify the similarity between Parathyroid and lymphocytic CD4. Serum PTH level was measured with an immunoradiometric assay in healthy control subjects and individuals with human immunodeficiency virus type 1. RESULTS: The parenchyma of normal and abnormal Parathyroid tissue displayed strikingly variable CD4 expression. Immunoprecipitation showed a 56 kd molecule, and Northern blot and polymerase chain reaction confirmed the similarity with lymphocyte CD4. Anti-Leu3a inhibited preferentially low calcium-stimulated secretion of PTH from dispersed Parathyroid Cells, without discernible influences on the cytoplasmic calcium concentration of these Cells. Individuals with human immunodeficiency virus type 1 displayed significantly lower serum PTH levels than healthy control subjects. CONCLUSIONS: The results suggest that the human Parathyroid Chief Cell expresses a CD4 moiety, which seems to interact in the PTH release in vitro and in vivo and which seems to use another second messenger system than the structurally similar T-Cell equivalent.
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Clinical characteristics and surgical treatment of sporadic primary hyperParathyroidism with emphasis on Chief Cell hyperplasia.
Surgery, 1990Co-Authors: C Wallfelt, Sverker Ljunghall, Reinhold Bergström, Jonas Rastad, Göran ÅkerströmAbstract:: In 570 patients with sporadic primary hyperParathyroidism, the age, sex, symptoms, and preoperative serum calcium values were related to the histopathologic diagnoses, operative findings, and the extent and outcome of Parathyroid surgery. Renal stone formation was especially prevalent in younger patients with slight hypercalcemia and Parathyroid Chief Cell hyperplasia, whereas neuromuscular and psychiatric disturbances were overrepresented among older women with higher serum calcium values. Serum calcium concentration was inversely correlated to the proportional incidence of Chief Cell hyperplasia and positively correlated to the glandular weight of both adenomas and hyperplasias. Glandular size was markedly irregular in Chief Cell hyperplasia, with increased gland weights of no more than two glands in 78% of patients. During follow-up, for as long as 27 years, normocalcemia was obtained in 91% of patients with adenomas, with failures mainly depending on difficulties in identifying the Parathyroid glands. The rate of normocalcemia was lower (80%) among patients with hyperplasia, but an inability to visualize the glands was not a major cause of failure. In patients with hyperplasia with asymmetric and more markedly enlarged glands, it appeared sufficient to remove only the enlarged glands, whereas the findings advocated a subtotal 3- to 3.5-gland resection in patients with more symmetrically or less enlarged hyperplastic glands.
Shawn T. Alexander - One of the best experts on this subject based on the ideXlab platform.
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Etelcalcetide, A Novel Calcimimetic, Prevents Vascular Calcification in A Rat Model of Renal Insufficiency with Secondary HyperParathyroidism
Calcified Tissue International, 2017Co-Authors: Longchuan Yu, James E. Tomlinson, Shawn T. Alexander, Kelly Hensley, Denise Dwyer, Marina Stolina, Charles Dean, William G. Goodman, William G. Richards, Xiaodong LiAbstract:Etelcalcetide, a novel peptide agonist of the calcium-sensing receptor, prevents vascular calcification in a rat model of renal insufficiency with secondary hyperParathyroidism. Vascular calcification occurs frequently in patients with chronic kidney disease (CKD) and is a consequence of impaired mineral homeostasis and secondary hyperParathyroidism (SHPT). Etelcalcetide substantially lowers Parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF23) levels in SHPT patients on hemodialysis. This study compared the effects of etelcalcetide and paricalcitol on vascular calcification in rats with adenine-induced CKD and SHPT. Uremia and SHPT were induced in male Wistar rats fed a diet supplemented with 0.75% adenine for 4 weeks. Rats were injected with vehicle, etelcalcetide, or paricalcitol for 4 weeks from the beginning of adenine diet. Rats fed an adenine-free diet were included as nonuremic controls. Similar reductions in plasma PTH and Parathyroid Chief Cell proliferation were observed in both etelcalcetide- and paricalcitol-treated rats. Serum calcium and phosphorus were significantly lower in etelcalcetide-treated uremic rats and was unchanged in paricalcitol-treated rats. Both serum FGF23 and aortic calcium content were significantly lower in etelcalcetide-treated uremic rats compared with either vehicle- or paricalcitol-treated uremic rats. The degree of aortic calcium content for etelcalcetide-treated rats was similar to that in nonuremic controls and corroborated findings of lack of histologic aortic mineralization in those groups. In conclusion, etelcalcetide and paricalcitol similarly attenuated progression of SHPT in an adenine rat model of CKD. However, etelcalcetide differentially prevented vascular calcification, at least in part, due to reductions in serum FGF23, calcium, and phosphorus levels.
Marina Stolina - One of the best experts on this subject based on the ideXlab platform.
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Etelcalcetide, A Novel Calcimimetic, Prevents Vascular Calcification in A Rat Model of Renal Insufficiency with Secondary HyperParathyroidism
Calcified Tissue International, 2017Co-Authors: Longchuan Yu, James E. Tomlinson, Shawn T. Alexander, Kelly Hensley, Denise Dwyer, Marina Stolina, Charles Dean, William G. Goodman, William G. Richards, Xiaodong LiAbstract:Etelcalcetide, a novel peptide agonist of the calcium-sensing receptor, prevents vascular calcification in a rat model of renal insufficiency with secondary hyperParathyroidism. Vascular calcification occurs frequently in patients with chronic kidney disease (CKD) and is a consequence of impaired mineral homeostasis and secondary hyperParathyroidism (SHPT). Etelcalcetide substantially lowers Parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF23) levels in SHPT patients on hemodialysis. This study compared the effects of etelcalcetide and paricalcitol on vascular calcification in rats with adenine-induced CKD and SHPT. Uremia and SHPT were induced in male Wistar rats fed a diet supplemented with 0.75% adenine for 4 weeks. Rats were injected with vehicle, etelcalcetide, or paricalcitol for 4 weeks from the beginning of adenine diet. Rats fed an adenine-free diet were included as nonuremic controls. Similar reductions in plasma PTH and Parathyroid Chief Cell proliferation were observed in both etelcalcetide- and paricalcitol-treated rats. Serum calcium and phosphorus were significantly lower in etelcalcetide-treated uremic rats and was unchanged in paricalcitol-treated rats. Both serum FGF23 and aortic calcium content were significantly lower in etelcalcetide-treated uremic rats compared with either vehicle- or paricalcitol-treated uremic rats. The degree of aortic calcium content for etelcalcetide-treated rats was similar to that in nonuremic controls and corroborated findings of lack of histologic aortic mineralization in those groups. In conclusion, etelcalcetide and paricalcitol similarly attenuated progression of SHPT in an adenine rat model of CKD. However, etelcalcetide differentially prevented vascular calcification, at least in part, due to reductions in serum FGF23, calcium, and phosphorus levels.
