Publications by authors named "G H Welsh"
Article Synopsis
- * Current treatments for CKD mainly focus on managing complications rather than addressing the root causes, indicating a need for personalized therapies targeting disease-related genes.
- * Advancements in understanding kidney-related genetic changes and successful gene therapies for specific cells have opened up new possibilities for improving kidney health through gene therapy and genome editing.
Article Synopsis
- * A retrospective study from 2010 to 2021 showed rates rose from 4.11 to 6.76 per 1000 total births after the new definition was implemented, resulting in an absolute increase of 2.58 stillbirths.
- * The increase in stillbirths was largely due to deaths associated with congenital anomalies and pregnancy terminations, with 37% of stillbirths being from fetuses under 500 g and 42% between 20 and 23 weeks gestation.
Background: Idiopathic nephrotic syndrome (INS) is a heterogenous disease and current classification is based on observational responses to therapies or kidney histology. The National Unified Renal Translational Research Enterprise (NURTuRE)-INS cohort aims to facilitate novel ways of stratifying INS patients to improve disease understanding, therapeutics and design of clinical trials.
Methods: NURTuRE-INS is a prospective cohort study of children and adults with INS in a linked biorepository.
Article Synopsis
- CRISPR-Cas technologies have transformed genetic engineering, showing potential in treating genetic diseases like chronic kidney disease (CKD), which can be caused by different mutations.
- Recent advances in genomic sequencing combined with CRISPR enable precise correction of mutations, especially in monogenic diseases, offering hope for treating conditions such as polycystic kidney disease and Alport syndrome.
- Innovations like prime editing and base editing improve genome editing efficiency and specificity without causing harmful DNA breaks, but challenges remain in developing effective delivery methods for therapies.
Insulin signaling to the glomerular podocyte via the insulin receptor (IR) is critical for kidney function. In this study we show that near-complete knockout of the closely related insulin-like growth factor 1 receptor (IGF1R) in podocytes is detrimental, resulting in albuminuria and podocyte cell death . In contrast, partial podocyte IGF1R knockdown confers protection against doxorubicin-induced podocyte injury.
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