J. A. Simpson

Muscle weakness and mitochondrial stress occur before metastasis in a novel mouse model of ovarian cancer cachexia

This paper introduces a novel mouse model of ovarian cancer cachexia showing that muscle weakness and mitochondrial stress occur before metastasis and atrophy in specific muscles.

Disrupted cardiac bioenergetics linked to oxidized mitochondrial creatine kinase are rescued by the mitochondrial-targeting peptide SBT-20 in the D2.mdx model of Duchenne muscular dystrophy

This paper investigates how mitochondrial bioenergetics are affected in D2.mdx mice and shows that SBT-20 can improve creatine-dependent bioenergetics by reducing oxidative stress.

Cardiac atrophy, dysfunction, and metabolic impairments: a cancer-induced heart failure phenotype

This study shows that cancer causes cardiac atrophy, dysfunction, and metabolic changes similar to heart failure in mouse models.

Characterisation of Plasmodium vivax lactate dehydrogenase dynamics in P. vivax infections

This study models PvLDH dynamics in P. vivax infections using Bayesian inference, finding significant differences between ex vivo and in vivo PvLDH levels and half-lives.

Seeking an optimal dosing regimen for OZ439-DSM265 combination therapy for treating uncomplicated falciparum malaria

This study uses a mathematical model to determine an optimal dosing regimen for OZ439-DSM265 combination therapy to treat uncomplicated falciparum malaria, predicting a regimen that cures 90% of patients within 42 days.

Investigating the efficacy of triple artemisinin-based combination therapies (TACTs) for treating Plasmodium falciparum malaria patients using mathematical modelling

This paper uses mathematical modeling to evaluate the efficacy of triple artemisinin-based combination therapy (TACT) against Plasmodium falciparum malaria, showing that adding mefloquine improves parasitological outcomes despite drug resistance.

Cellular Interplay and Cytokine Hierarchy Cause Pathological Cardiac Hypertrophy in RAF1-Mutant Noonan Syndrome

This study shows that RAF1 mutations in Noonan syndrome cause cardiac hypertrophy through cytokine signaling from endothelial cells, with TNF/IL6 as potential therapeutic targets.