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Introduction: Recently, bone-active factors such as parathyroid hormone and lactoferrin, have been used in pre-clinical models to promote tendon healing. How-ever, there is limited understanding of how these boneactive factors may affect the cells of the ten-don themselves. Here, we present an in vitro study assessing the effects of parathyroid hor-mone and lactoferrin on primary tendon cells (tenocytes), and compare their responses to the tenogenic factors, PDGF, IGF-1 and TGF-β.
Materials And Methods: Tenocyte proliferation and collagen production were assessed by alamarBlue® and Sirius red as-says, respectively. To assess tenocyte trans-differentiation, changes in the expression of genes important in tenocyte, chondrocyte and osteoblast biology were determined using real-time PCR.
Results: Parathyroid hormone and lactoferrin had no effect on tenocyte growth or collagen production, with minimal changes in gene expression and no detrimental effects observed to suggest trans-differentiation away from tendon cell behaviour. Tenogenic factors PDGF, IGF-1 and TGF all increasetenocyte collagen production, however, the gene expression data suggests that PDGF promotes severe de-differentiation of the tenocytes.
Discussion: Our findings suggest that using parathyroid hormone or lactoferrin as a singular factor to promote tendon healing may not be of benefit, but for use in tendon-bone healing there would be no detrimental effect on the tendon itself.
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http://dx.doi.org/10.11138/mltj/2017.7.2.215 | DOI Listing |
BMJ Case Rep
September 2025
Diabetes and Endocrinology, North West Anglia NHS Foundation Trust, Peterborough, Cambridgeshire, UK
Familial hypocalciuric hypercalcaemia (FHH) is a rare disorder that represents a minute but important part of the differential diagnosis of hypercalcaemia. We describe a man in his 60s who was re-referred to endocrinology because of hypercalcaemia thought to be due to primary hyperparathyroidism (PHPT) that had not been followed up for 13 years. In his early 50s, the hypercalcaemia was accompanied by normal serum parathyroid hormone (PTH) levels, normal 24-hour urinary calcium excretion and normal bone density and kidney imaging, and no parathyroid adenoma was demonstrated on neck imaging.
View Article and Find Full Text PDFArq Bras Cardiol
September 2025
Escola Bahiana de Medicina e Saúde Pública, Salvador, BA - Brasil.
Background: Chronic kidney disease (CKD) is associated with a higher prevalence of valvular diseases and increased mortality from cardiovascular causes. Factors that influence the genesis of cardiac valve calcification (CVC) in these patients are not well-defined.
Objective: To determine the risk factors for valvular calcification in patients with CKD.
Cureus
August 2025
Biochemistry, Liaquat University of Medical and Health Sciences, Karachi, PAK.
Background: Vitamin D insufficiency is increasingly recognized as a significant and underlying contributor to a wide range of musculoskeletal disorders, particularly in gastrointestinal (GI) and endocrine health. The study aims to determine the clinical relationship between vitamin D status and the severity of GI symptoms, while also assessing the impact of related endocrine disturbances.
Methods: A cross-sectional study was conducted involving 120 adult patients with GI problems, including constipation, bloating, irritable bowel syndrome (IBS), and dyspepsia in a tertiary care hospital over a six-month duration.
Handb Exp Pharmacol
September 2025
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Research conducted over the last 15 years indicates that cAMP is generated not just from the plasma membrane but also from intracellular compartments, particularly in endosomes, where receptors are redistributed during the endocytosis process. This review centers on the parathyroid hormone type 1 receptor (PTHR) as a model for a peptide hormone GPCRs that generates cAMP from various locations with distinct duration and pharmacological effectiveness. We discuss how structural dynamics simulations aid in designing ligands that induce cAMP location bias, ultimately answering how the spatiotemporal generation of cAMP affects pharmacological responses mediated by the PTHR.
View Article and Find Full Text PDFOsteoporos Int
September 2025
Molecular Bone Histology Lab, Research Unit of Pathology, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Intermittent PTH treatment has been used as both an osteoanabolic treatment in osteoporosis and a hormone replacement in hypoparathyroidism for many years. This scoping review compiles and reinterprets studies using histomorphometry supported by bone turnover markers to investigate the elusive cellular effect of intermittent PTH treatment locally within the bone, while illuminating knowledge gaps. Intermittent PTH increases both osteoclast and osteoblast activity within the first 6 months of treatment.
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