Publications by authors named "O A Dawodu"

Article Synopsis
  • Mutations causing premature termination codons (PTCs) in protein-coding genes lead to severe, often life-threatening genetic diseases that currently lack approved treatments.
  • Scientists are exploring suppressor tRNAs (sup-tRNAs) that could potentially translate these PTCs and restore protein synthesis, but developing efficient and specific sup-tRNAs is challenging.
  • This research introduces a new approach using a naturally occurring pyrrolysine tRNA (tRNAPyl) to create a series of engineered suppressor tRNAs (PASS-tRNAs), which successfully restored protein synthesis in both bacterial and human cells, showing promise for treating genetic disorders like BRCA1 mutations in cancer.
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Introduction: Fetus in fetu is a paediatric rarity. It involves the presence of a mass resembling a fetus inside the body of a child or an adult. It is described as a twin growing inside the body of the other.

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Introduction: trichoscopic and histopathological evaluation of non-scarring systemic lupus erythematosus (SLE) alopecia is uncommon. We aimed to document the prevalence, pattern of hair loss, trichoscopic and histopathologic differences between systemic lupus erythematosus patients with and without hair loss.

Methods: this was a cross-sectional comparative study of 75 systemic lupus erythematosus patients, 36 with hair loss from February to December 2020.

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Objective: To determine the frequency, demography, aetiology and mechanisms of ocular injuries associated with childhood traumatic cataract in Nigeria.

Methods: A retrospective multicentre study conducted across ten child eye health tertiary facilities in Nigeria between January 2017 and December 2021. Clinic records of all children aged 0-17 years who had been diagnosed with cataract at the various participating centres were reviewed.

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Targeting of the multifunctional enzyme apurinic/apyrimidinic endonuclease I/redox factor 1 (APE1) has produced small molecule inhibitors of both its endonuclease and redox activities. While one of the small molecules, the redox inhibitor APX3330, completed a Phase I clinical trial for solid tumors and a Phase II clinical trial for Diabetic Retinopathy/Diabetic Macular Edema, the mechanism of action for this drug has yet to be fully understood. Here, we demonstrate through HSQC NMR studies that APX3330 induces chemical shift perturbations (CSPs) of both surface and internal residues in a concentration-dependent manner, with a cluster of surface residues defining a small pocket on the opposite face from the endonuclease active site of APE1.

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