The repair of oxidatively damaged proteins by the newly discovered activity in YjbI is important for the adaptation of Bacillus subtilis to oxidative environments.

The structure of the trypanosome haptoglobin-haemoglobin receptor bound to its ligand reveals the molecular basis for ligand recognition in innate immunity and identifies molecular determinants that aid efficient uptake.

Genetic analysis identifies an enzyme of the malaria parasite that is required to seal its host red blood cell membrane upon invasion, a key requirement of this important intracellular pathogen.

In silico modelling of all available data shows that a twenty-day ascending-dose primaquine regimen could be safe to administer to G6PD deficient patients for the radical cure of vivax malaria.

The rhoptry protein RhopH3 is crucial for the invasion and growth of the malaria parasite and disruption of it provides insight into the binding of the parasite to the host red blood cell and into the formation of new import pathways.

Fibrinogen, a key protein involved in blood coagulation, contains a disordered and previously poorly characterised region called αC that plays a critical role in fibrin fibre growth and clot stability.

Elevated growth differentiation factor-15 (GDF15) levels do not appear to be a causal factor in body mass index (BMI) in humans but higher BMI does cause increases in GDF15.

Sleep-related hemodynamic signals are much larger than those in the awake brain, so it is crucial to monitor the arousal state during studies of spontaneous activity.

Insights into the basic metabolic architecture and adaptations of malaria parasites for growth within human erythrocytes exemplify how incisive knowledge of biochemical pathways and mechanisms may be leveraged to develop new therapies.