Publications by authors named "Sreyanko Sadhukhan"
Chronic kidney disease-induced secondary hyperparathyroidism (CKD-SHPT) heightens fracture risk through impaired mineral homeostasis and elevated levels of uremic toxins (UTs), which in turn enhance bone remodeling. Etelcalcetide (Etel), a calcium-sensing receptor (CaSR) agonist, suppresses parathyroid hormone (PTH) in hyperparathyroidism to reduce excessive bone resorption, leading to increased bone mass. However, Etel's effect on bone quality, chemical composition, and strength is not well understood.
View Article and Find Full Text PDFPurpose: Runx2 and osteocalcin have pivotal roles in bone homeostasis. Polymorphism of these two genes could alter the function of osteoblasts and consequently bone mineral density (BMD). Attempts to understand the relationship between these polymorphisms and BMD in postmenopausal women across a variety of populations have yielded inconsistent results.
View Article and Find Full Text PDFPurpose: To understand the pathophysiology of idiopathic osteoporosis (IOP) better, we conducted a systematic review and meta-analysis of bone mineral density (BMD), hormones, and bone turnover markers (BTMs) between IOP patients and healthy controls.
Methods: Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, an appropriate search query was created, and three databases, including PubMed, ScienceDirect, and Google Scholar, were searched for screening relevant original articles. Feasible information, both qualitative and quantitative, was extracted and used to conduct meta-analyses.
Article Synopsis
- This study examined how hormonal (combined hormonal contraceptive, CHC) and non-hormonal (ormeloxifene, NHC) oral contraceptives affect bone properties in pubertal female rats over 3 and 7 months.
- Results showed that while NHC initially improved bone mass after 3 months, both types of OCs led to reduced bone mass and weakened bone structure after 7 months.
- NHC had a lesser impact compared to CHC, which significantly compromised bone strength and increased the risk of micro-damage and fractures.
Article Synopsis
- Excess nitric oxide (NO) produced in response to inflammation can lead to various diseases, and current treatment methods targeting its production have not been successful.
- Urea-functionalized push-pull chromophores, like 1,1,4,4-tetracyanobuta-1,3-dienes (TCBD) and expanded TCBD (eTCBD), have been developed to scavenge excess NO, converting it into stable NONOates upon binding.
- Urea-eTCBD not only serves as a NO sensor but also effectively inactivates NO in inflammatory conditions, demonstrating therapeutic potential in animal models and providing a basis for further research on similar compounds.
Introduction: In obese humans, root extract (CF) protects against weight gain owing to the presence of forskolin, an adenylate cyclase (AC) activator. As AC increases intracellular cyclic adenosine monophosphate (cAMP) levels in osteoblasts that has an osteogenic effect, we thus tested the skeletal effects of a standardized CF (CFE) in rats.
Methods: Concentrations of forskolin and isoforskolin were measured in CFE by HPLC.
Early diagnosis of hypophosphatasia (HPP) is challenging. Here, we propose to broaden the diagnostic criteria of HPP by reviewing published data on BMD and fractures in HPP patients. Non-osteoporotic fractures and higher than normal lumbar BMD were recurrent in HPP patients and could be included as diagnostic criteria.
View Article and Find Full Text PDF