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Introduction: Sotalol is a beta-adrenoceptor blocking drug with unique physical and pharmacologic properties. Unlike most beta-adrenoceptor blocking drugs, sotalol is amenable to extracorporeal removal and causes QT interval prolongation and ventricular dysrhythmias. These properties have implications for treating sotalol poisoning.

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Background: 17α-Hydroxylase/17,20-lyase deficiency (17OHD) is a rare form of congenital adrenal hyperplasia (CAH), caused by mutations in the CYP17A1 gene. It typically manifests clinically as variable degree of hypertension, hypokalemia, and disorders of sexual development (DSD), which can include abnormal sexual differentiation in males and sexual infantilism in females. Over 100 mutations in CYP17A1 have been identified, with most cases involving missense mutations or small deletions.

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Background: Primary aldosteronism (PA) is the leading surgically treatable cause of hypertension, with adrenalectomy as the definitive treatment for unilateral PA (UPA). However, some patients have persistent hypertension after surgery. This study aims to identify preoperative factors affecting surgical outcomes and develop a predictive model for postoperative hypertension resolution.

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This review explores the therapeutic potential of the stable gastric pentadecapeptide BPC 157 in addressing electrolyte imbalances, specifically hyperkalemia, hypokalemia, hypermagnesemia, and hyperlithemia. In hyperkalemia, BPC 157 demonstrated a comprehensive counteractive effect against KCl overdose (intraperitoneally, intragastrically, and in vitro), effectively mitigating symptoms such as muscular weakness, hypertension, sphincter dysfunction, arrhythmias, and lethality. It also counteracted the adverse effects of succinylcholine and magnesium overdose, including systemic muscle paralysis, arrhythmias, and hyperkalemia.

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A forward genetic screen identifies potassium channel essentiality in SHH medulloblastoma maintenance.

Dev Cell

January 2025

Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Arthur and Sonia Labatt Brain Tumour Research Centre, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada. Electronic address:

Distinguishing tumor maintenance genes from initiation, progression, and passenger genes is critical for developing effective therapies. We employed a functional genomic approach using the Lazy Piggy transposon to identify tumor maintenance genes in vivo and applied this to sonic hedgehog (SHH) medulloblastoma (MB). Combining Lazy Piggy screening in mice and transcriptomic profiling of human MB, we identified the voltage-gated potassium channel KCNB2 as a candidate maintenance driver.

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