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Hasemer, H.

Publications and source records attributed to Hasemer, H..

2 recordsLinked to original sources

Stabilisation of soil organic matter with rock dust partially counteracted by plants

Soil application of Ca- and Mg-rich silicates can capture and store atmospheric carbon dioxide as inorganic carbon but could also have the potential to stabilise soil organic matter (SOM). Synergies between these two processes have not been investigated. Here, we apply finely ground silicate rock mining residues (basalt and granite blend) to a loamy sand in a pot trial at a rate of 4% (equivalent to 50 t ha-1) and investigate the effects of a wheat plant and two watering regimes on soil carbon sequestration. Rock dust addition increased soil pH, electric conductivity and soil-exchangeable Ca and Mg contents, as expected for weathering, but decreased exchangeable levels of micronutrients Mn and Zn, likely related to soil pH. Importantly, it increased mineral-associated organic matter by 22% due to the supply of secondary minerals and associated sites for SOM sorption. Additionally, in the non-planted treatments, rock supply of Ca and Mg increased soil microaggregation that subsequently stabilised labile particulate organic matter as organic matter occluded in aggregates by 46%. Plants, however, reduced soil exchangeable Mg and Ca contents and hence counteracted the silicate rock effect on microaggregates and carbon within. We attribute this cation loss to plant exudates released to solubilise micronutrients and hence neutralise plant deficiencies. The effect of enhanced silicate rock weathering on SOM stabilisation could substantially boost its carbon sequestration potential when pH and micronutrient effects are considered.

plant biology↗

Generation and characterisation of P. falciparum parasites with a G358S mutation in the PfATP4 Na+ pump and clinically relevant levels of resistance to some PfATP4 inhibitors

Small-molecule inhibitors of PfATP4, a Plasmodium falciparum protein that is believed to pump Na+ out of the parasite while importing H+, are on track to become much-needed new antimalarial drugs. The spiroindolone cipargamin is poised to become the first PfATP4 inhibitor to reach the field, having performed strongly in Phase 1 and 2 clinical trials. Previous attempts to generate cipargamin-resistant parasites in the laboratory have yielded parasites with reduced susceptibility to the drug; however, the highest 50% inhibitory concentration reported to date is 24 nM. Here, we show that P. falciparum parasites can acquire a clinically-significant level of resistance to cipargamin that enables them to withstand micromolar concentrations of the drug. Independent experiments to generate high-level cipargamin resistance using different protocols and strains led to the same change each time - a G358S mutation in PfATP4. Parasites with this mutation showed high-level resistance not only to cipargamin, but also to the dihydroisoquinolone (+)-SJ733. However, for certain other (less clinically advanced) PfATP4-associated compounds the G358S mutation in PfATP4 conferred only moderate resistance or no resistance. The G358S mutation in PfATP4 did not affect parasite susceptibility to antimalarials that do not target PfATP4. The G358S mutation in PfATP4, and the equivalent mutation in the Toxoplasma gondii ATP4 homologue (G419S), decreased the sensitivity of the Na+-ATPase activity of ATP4 to inhibition by cipargamin and (+)-SJ733, and decreased the sensitivity of parasites expressing these ATP4 mutations to disruption of parasite Na+ regulation by cipargamin- and (+)-SJ733. The G358S mutation in PfATP4 reduced the affinity of the protein for Na+ and was associated with an increase in the parasites resting cytosolic Na+ concentration; however, no significant defect in parasite growth rate was observed. Our findings suggest that codon 358 in pfatp4 should be monitored closely in the field as a molecular marker for cipargamin resistance, and that PfATP4 inhibitors in clinical development should be tested for their activity against PfATP4G358S parasites.

microbiology↗