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Correction to: Long-term safety and effectiveness of a somatropin biosimilar (Omnitrope®) in children requiring growth hormone therapy: analysis of final data of Italian patients enrolled in the PATRO children study.
Endocrine
January 2025
Pediatric Unit, IRCCS AOU of Bologna, Bologna, Italy.
Adenine base editor corrected ADPKD point mutations in hiPSCs and kidney organoids.
Adv Biotechnol (Singap)
June 2024
MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, Guangdong, 510275, China.
Autosomal dominant polycystic kidney disease (ADPKD) is a dominant genetic disorder caused primarily by mutations in the PKD1 gene, resulting in the formation of numerous cysts and eventually kidney failure. However, there are currently no gene therapy studies aimed at correcting PKD1 gene mutations. In this study, we identified two mutation sites associated with ADPKD, c.
View Article and Find Full Text PDFHigher bone mineral density at six years of age in very preterm-born infants fed human milk compared to formula feeding. A secondary analysis of an RCT.
Eur J Pediatr
January 2025
Institute of Clinical Research, University of Southern Denmark, Odense, Denmark.
Unlabelled: In very preterm-born infants, nutritional intake is important to reduce the risk of severe metabolic bone disease including the risk of a lower bone mineral density (BMD). The aim of this study was to evaluate bone mineral content (BMC) and BMD (measured as BMC per bone area (BA)) at six years of age in very preterm-born infants fed different diets post-discharge. Data on this topic so far is insufficient, and with this study we aim to supply more useful data.
View Article and Find Full Text PDFFirst branchial cleft anomalies in children: long-term outcome in 16 patients.
Eur Arch Otorhinolaryngol
January 2025
Otorhinolaryngology, Head and Neck Surgery, University Hospitals Leuven, Leuven, Belgium.
Introduction: First branchial cleft anomalies (FBCA) are rare congenital head and neck malformations, often subject to incorrect diagnosis and treatment. We present our experience with FBCA, focusing on clinical presentation, diagnosis, perioperative relation to the facial nerve, surgical approach, complications and patient satisfaction.
Methods: A consecutive cohort of 16 patients undergoing surgical treatment for FBCA between 1999 and 2021 was analyzed.
Retinoid-impregnated nanoparticles enable control of bone growth by site-specific modulation of endochondral ossification in mice.
J Bone Miner Res
January 2025
Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, MD.
Growth-plate (GP) injures in limbs and other sites can impair GP function and cause deceleration of bone growth, leading to progressive bone lengthening imbalance, deformities and/or physical discomfort, decreased motion and pain. At present, surgical interventions are the only means available to correct these conditions by suppressing the GP activity in the unaffected limb and/or other bones in the ipsilateral region. Here, we aimed to develop a pharmacologic treatment of GP growth imbalance that involves local application of nanoparticles-based controlled release of a selective retinoic acid nuclear receptor gamma (RARγ) agonist drug.
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