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Ophthalmic Complications Associated With the Antidiabetic Drugs Semaglutide and Tirzepatide.
JAMA Ophthalmol
January 2025
John A. Moran Eye Center, Department of Ophthalmology & Visual Sciences, Department of Neurology, University of Utah Health, Salt Lake City.
Importance: Nearly 2% of the US population received a prescription for semaglutide in 2023. There has been a recent concern that this drug and other similar medications may be associated with ophthalmic complications.
Objective: To report ophthalmic complications associated with the use of semaglutide or tirzepatide.
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
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Pediatric Unit, IRCCS AOU of Bologna, Bologna, Italy.
Nanoparticles-Based Optical Chemosensors for Lead Acetate Sensing in Water: ZnO, ZnCeO, and ZnNdO.
J Fluoresc
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Materials Science Lab (1), Physics Department, Faculty of Science, Cairo University, Giza, Egypt.
This study reports the synthesis, characterization, and optical properties of ZnO, ZnCeO, and ZnNdO nanoparticles and their interactions with lead acetate solutions. X-ray diffraction (XRD) confirmed that the nanoparticles were synthesized in a single-phase hexagonal structure, with crystallite sizes of 12.48 nm, 50.
View Article and Find Full Text PDFTherapeutic gene correction of HBB frameshift CD41-42 (-TCTT) deletion in human hematopoietic stem cells.
Adv Biotechnol (Singap)
January 2025
MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, 510275, Guangdong, China.
Β-thalassemia is one of the global health burdens. The CD41-42 (-TCTT) mutation at HBB is the most prevalent pathogenic mutation of β-thalassemia in both China and Southeast Asia. Previous studies focused on repairing the HBB CD41-42 (-TCTT) mutation in β-thalassemia patient-specific induced pluripotent stem cells, which were subsequently differentiated into hematopoietic stem and progenitor cells (HSPCs) for transplantation.
View Article and Find Full Text PDFAdenine 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.
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