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PTH Related Peptide, aa 107_111, Osteostatin, Sheep anti_Human; ELISA

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[#YIA4242.1] PTH Related Peptide, aa 107_111, Osteostatin, Sheep anti_Human; ELISA


YIA4242.1 | PTH Related Peptide, aa 107_111, Osteostatin, Sheep anti_Human; ELISA, 20 µl.
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(1) Two cases of humoral hypercalcemia of malignancy complicating infantile fibrosarcoma.[TOP]

Pubmed ID :28371408
Publication Date : //
We report two infants with infantile fibrosarcoma (IFS) complicated by severe hypercalcemia. Assessment demonstrated suppressed parathyroid hormone and 1,25-dihydroxyvitamin D levels with elevated circulating levels of parathyroid hormone related protein, indicating the diagnosis of humoral hypercalcemia of malignancy (HHM). HHM is a paraneoplastic syndrome rarely associated with pediatric malignancies. Hypercalcemia manifested clinically with neurologic symptoms and soft tissue calcium deposition and required aggressive management with intravenous fluids, diuretics, and supplemental electrolytes. Following treatment with neoadjuvant chemotherapy, serum calcium levels precipitously declined requiring calcium repletion. These cases highlight the improvement of hypercalcemia secondary to HHM following chemotherapy.

Authors : Hirschfeld Ryan, Welch Jennifer J G, Harrison Douglas J, Kremsdorf Robin, Chawla Anjulika,

(2) Heterotrimeric G proteins in the control of parathyroid hormone actions.[TOP]

Pubmed ID :28363951
Publication Date : //
Parathyroid hormone (PTH) is a key regulator of skeletal physiology and calcium and phosphate homeostasis. It acts on bone and kidney to stimulate bone turnover, increase the circulating levels of 1,25 dihydroxyvitamin D and calcium and inhibit the reabsorption of phosphate from the glomerular filtrate. Dysregulated PTH actions contribute to or are the cause of several endocrine disorders. This calciotropic hormone exerts its actions via binding to the PTH/PTH-related peptide receptor (PTH1R), which couples to multiple heterotrimeric G proteins, including G and G Genetic mutations affecting the activity or expression of the alpha-subunit of G, encoded by the complex locus, are responsible for several human diseases for which the clinical findings result, at least partly, from aberrant PTH signaling. Here, we review the bone and renal actions of PTH with respect to the different signaling pathways downstream of these G proteins, as well as the disorders caused by mutations.

Authors : Bastepe Murat, Turan Serap, He Qing,

(3) Parathyroid Hormone and Parathyroid Hormone-Related Protein Analogs in Osteoporosis Therapy.[TOP]

Pubmed ID :28303448
Publication Date : //
The purpose is to review the efficacy and optimal use of parathyroid hormone and parathyroid hormone-related protein analogs in osteoporosis treatment.

Authors : Leder Benjamin Z,

(4) Serum NT-proBNP Levels Are Not Related to Vitamin D Status in Young Patients with Congenital Heart Defects.[TOP]

Pubmed ID :26955207
Publication Date : //
Hypovitaminosis D frequently occurs in early life and increases with age. Vitamin D has been suggested to influence cardiac performance and N-terminal-pro-type B natriuretic peptide (NT-proBNP) release in adults with heart failure.

Authors : Passeri E, Rigolini R, Costa E, Verdelli C, Arcidiacono C, Carminati M, Corbetta S,

(5) Relation of Age, Sex and Bone Mineral Density to Serum 25-Hydroxyvitamin D Levels in Chinese Women and Men.[TOP]

Pubmed ID :26791959
Publication Date : //
To investigate the relation of circulating 25-hydroxyvitamin D (25[OH]D) levels to age, sex, and bone mineral density (BMD) in adults living in Guangzhou Province.

Authors : Wei Qiu-shi, Chen Zhen-qiu, Tan Xin, Su Hai-rong, Chen Xiao-xiang, He Wei, Deng Wei-min,

(6) Comparative study of the effect of PTH (1-84) and strontium ranelate in an experimental model of atrophic nonunion.[TOP]

Pubmed ID :26521993
Publication Date : //
This study aimed to set up an experimental model of long bone atrophic nonunion and to explore the potential role of PTH-1-84 (PTH 1-84) and strontium ranelate (SrR). A model of atrophic nonunion was created in Sprague-Dawley rats at the femoral midshaft level. The animals were randomised into four groups. Group A1: control rodents, fracture without bone gap; Group A2: rodents with subtraction osteotomy (non-union model control) treated with saline; Group B: rodents with subtraction osteotomy treated with human-PTH (PTH 1-84); and Group C: rodents with subtraction osteotomy treated with strontium ranelate (SrR). The groups were followed for 12 weeks. X-rays were be obtained at weeks 1, 6 and 12. After sacrificing the animals, we proceeded to the biomechanical study and four point bending tests to evaluate the resistance of the callus and histological study. In second phase, the expression of genes related to osteoblast function was analysed by reverse transcription-quantitative PCR in rats subjected to substraction osteotomy and treated for 2 weeks. The animals were randomised into three groups: Group A2: rodents treated with saline; Group B: rodents treated with PTH 1-84 and Group C: rodents treated with SrR.

Authors : Pérez Núñez M I, Ferreño Blanco D, Alfonso Fernández A, Casado de Prado J A, Sánchez Crespo M, De la Red Gallego M, Pascual Carra A, Rodriguez López T, Diego Cavia S, Garcés Zarzalejo C, Mayorga Fernández M, Ruiz Martínez E, Carrascal Vaquero I, Riancho Moral J A,

(7) Voyages of Discovery.[TOP]

Pubmed ID :26138832
Publication Date : //
The metabolism of calcium and bone is controlled by five principal hormones: parathyroid hormone, 1,25-dihydroxyvitamin D, calcitonin, parathyroid hormone-related peptide and fibroblast growth factor 23, some of which have been known for several decades and some of which have only more recently been identified. The stories of the discovery of these hormones have constituted a series of complex journeys that have been undertaken over the past century or so, none of which has yet been completed. The complexities of bone and calcium metabolism have been and remain, to many people, somewhat mysterious and a daunting task to understand. This book is designed to try to unravel those mysteries and present them in an interesting and comprehensible manner.

Authors : Allgrove Jeremy,

(8) Associations between frailty and serum N-terminal propeptide of type I procollagen and 25-hydroxyvitamin D in older Spanish women: The Toledo Study for Healthy Aging.[TOP]

Pubmed ID :26031553
Publication Date : //
Frail older people are at high risk for fractures and falls increasing the rates of institutionalization and mortality. Bone markers have been related to both aging and fractures. However, no previous reports have shown a potential relationship between serum bone markers such as N-terminal propeptide of type I procollagen (PINP), C-terminal telopeptide of type I collagen (β-CTX) and parathyroid hormone (PTH) with frailty in elderly female populations. This study is aimed at examining the associations of bone metabolism markers and frailty in older Spanish women through a descriptive cross-sectional analysis based on a cohort of the Toledo Study for Healthy Aging (TSHA). The levels of serum PINP, β-CTX, PTH and 25-hydroxyvitamin D (25(OH)D) were assessed in 592 participants (median age 74years) who were defined as robust, prefrail and frail according to Fried's approach. Frail subjects had significantly high levels of PINP, β-CTX and PTH and low production of 25(OH)D. After adjustment for confounders, high PINP levels (defined by the upper quartile) and low levels of 25(OH)D (lower quartile) remained significantly associated to frailty [OR for PINP: 2.19 (95% CI, 1.15-4.18; P=0.017); OR for 25(OH)D: 1.65 (95% CI, 1.02-2.67; P=0.042)]. Women with both high PINP levels and low 25(OH)D levels presented a 5.85-fold increased frailty risk (95% CI, 1.64-20.93; P=0.007). The main contribution of this paper is the novel definition of PINP and 25(OH)D markers as potential biomarkers of frailty and targets for intervention.

Authors : Alvarez-Ríos Ana I, Guerrero Juan M, García-García Francisco J, Rodríguez-Mañas Leocadio, Medrano-Campillo Pablo, de la Torre Lanza María A, Alvarez-Sánchez Nuria, Carrillo-Vico Antonio,

(9) 15-deoxy-δ12,14-prostaglandin j2 inhibits osteolytic breast cancer bone metastasis and estrogen deficiency-induced bone loss.[TOP]

Pubmed ID :25859665
Publication Date : //
Breast cancer is the major cause of cancer death in women worldwide. The most common site of metastasis is bone. Bone metastases obstruct the normal bone remodeling process and aberrantly enhance osteoclast-mediated bone resorption, which results in osteolytic lesions. 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is an endogenous ligand of peroxisome proliferator-activated receptor gamma (PPARγ) that has anti-inflammatory and antitumor activity at micromolar concentrations through PPARγ-dependent and/or PPARγ-independent pathways. We investigated the inhibitory activity of 15d-PGJ2 on the bone loss that is associated with breast cancer bone metastasis and estrogen deficiency caused by cancer treatment. 15d-PGJ2 dose-dependently inhibited viability, migration, invasion, and parathyroid hormone-related protein (PTHrP) production in MDA-MB-231 breast cancer cells. 15d-PGJ2 suppressed receptor activator of nuclear factor kappa-B ligand (RANKL) mRNA levels and normalized osteoprotegerin (OPG) mRNA levels in hFOB1.19 osteoblastic cells treated with culture medium from MDA-MB-231 cells or PTHrP, which decreased the RANKL/OPG ratio. 15d-PGJ2 blocked RANKL-induced osteoclastogenesis and inhibited the formation of resorption pits by decreasing the activities of cathepsin K and matrix metalloproteinases, which are secreted by mature osteoclasts. 15d-PGJ2 exerted its effects on breast cancer and bone cells via PPARγ-independent pathways. In Balb/c nu/nu mice that received an intracardiac injection of MDA-MB-231 cells, subcutaneously injected 15d-PGJ2 substantially decreased metastatic progression, cancer cell-mediated bone destruction in femora, tibiae, and mandibles, and serum PTHrP levels. 15d-PGJ2 prevented the destruction of femoral trabecular structures in estrogen-deprived ICR mice as measured by bone morphometric parameters and serum biochemical data. Therefore, 15d-PGJ2 may be beneficial for the prevention and treatment of breast cancer-associated bone diseases.

Authors : Kim Ki Rim, Kim Hyun Jeong, Lee Sun Kyoung, Ma Gwang Taek, Park Kwang Kyun, Chung Won Yoon,

(10) Synergistic effects of high dietary calcium and exogenous parathyroid hormone in promoting osteoblastic bone formation in mice.[TOP]

Pubmed ID :25744000
Publication Date : //
In the present study, we investigated whether high dietary Ca and exogenous parathyroid hormone 1-34 fragments (PTH 1-34) have synergistic effects on bone formation in adult mice, and explored the related mechanisms. Adult male mice were fed a normal diet, a high-Ca diet, a PTH-treated diet, or a high-Ca diet combined with subcutaneously injected PTH 1-34 (80 μg/kg per d) for 4 weeks. Bone mineral density, trabecular bone volume, osteoblast number, alkaline phosphatase (ALP)- and type I collagen-positive areas, and the expression levels of osteoblastic bone formation-related genes and proteins were increased significantly in mice fed the high-Ca diet, the PTH-treated diet, and, even more dramatically, the high-Ca diet combined with PTH. Osteoclast number and surface and the ratio of receptor activator for nuclear factor-κB ligand (RANKL):osteoprotegerin (OPG) were decreased in the high-Ca diet treatment group, increased in the PTH treatment group, but not in the combined treatment group. Furthermore, third-passage osteoblasts were treated with high Ca (5 mM), PTH 1-34 (10⁻⁸ M) or high Ca combined with PTH 1-34. Osteoblast viability and ALP activity were increased in either the high Ca-treated or PTH-treated cultures and, even more dramatically, in the cultures treated with high Ca plus PTH, with consistent up-regulation of the expression levels of osteoblast proliferation and differentiation-related genes and proteins. These results indicate that dietary Ca and PTH play synergistic roles in promoting osteoblastic bone formation by stimulating osteoblast proliferation and differentiation.

Authors : Feng Yuxu, Zhou Min, Zhang Qunhu, Liu Huan, Xu Yong, Shu Lei, Zhang Jue, Miao Dengshun, Ren Yongxin,