Immobilisation of phosphorus by iron-coated roots of submerged macrophytes

Hydrobiologia - To observe effects on the phosphorus retention mechanisms of a lake after re-colonisation by macrophytes, Potamogeton crispus L. and Elodea canadensis Michx. were planted in lab...     

Long-term effects of dietary isoflavones on uterine gene expression profiles

Isoflavones (ISOs) are bioactive food ingredients of the traditional East Asian diet and currently discussed as alternatives to classical hormone replacement therapies and for reducing the prevalence of hormone-dependent cancers. Although there are many studies on ISOs, not much is known about their long-term effects.Therefore, we performed an animal experiment analyzing the effects of three different diets: a phytoestrogen-free diet, a diet supplemented with genistein (700 μg/g diet) and an ISO-high diet (232 μg daidzein and 240 μg genistein/g) at two distinct time points, juvenile (21 days) and adult (97 days). Exposure started prior to mating of the parents and throughout the life of the offspring.We observed a stronger increase of uterine wet weights in juvenile offspring with genistein exposure (1018 ± 350 mg/kg BW) than with ISO-high diet (497 ± 133 mg/kg BW). Whereas the expression of proliferation related genes (PCNA; Ki67; IGF-1; IGF-1R), analyzed by real-time-qPCR and Western blot, were significantly down-regulated in juvenile animals exposed to genistein. Additionally, genistein exposure led to estrogenic responses, observed upon increase of complement C3 and decrease of estrogen receptors gene expressions, while the exposure to ISO-high diet did not show these effects.In conclusion, both the time point on which phytoestrogen exposure starts together with the composition of the ingested phytoestrogen containing diet are of great importance for the biological response of the offspring.     

Methane oxidation by methanotrophs and its effects on the phosphate flux over the sediment-water interface in a eutrophic lake

The effect of methane oxidation in aerobic sediment on oxygen consumption and phosphate flux was investigated in diffusion chambers. The diffusion chambers consisted of two compartments separated by a Teflon membrane. In the upper chamber a thin sediment layer was present and the lower chamber was continuously flushed with gas. The hydrophobic membrane allowed for diffusion of gases from the lower chamber through the sediment layer toward the headspace of the upper chamber. In experiments with a methane oxidation rate of 9.8 mmol m^–2 day^–1, the oxygen consumption rate increased by a factor of two compared with controls without methane oxidation (8.6 vs 17.7 mmol m^–2 day^–1). Methane oxidation significantly decreased oxygen penetration depth (2.5–4.0 vs 1.0–2.0 mm). However, despite the shrinkage of the oxidized microlayer, no differences were found in phosphate flux across the sediment water interface. Batch experiments with standard additions of methane revealed that the growth of methanotrophic bacteria contributes to the phosphate uptake of aerobic sediment. From the batch experiments a molar ratio of carbon to phosphate of 45 mol:mol was calculated for the growth of methanotrophs. Results suggest that a decrease in chemical phosphate adsorption caused by a decrease in the oxygen penetration depth could be compensated for entirely by the growth of methanotrophic bacteria. Send offprint requests to: A.J.C. Sinke     

A locus for familial hypertrophic cardiomyopathy is closely linked to the cardiac myosin heavy chain genes, CRI-L436, and CRI-L329 on chromosome 14 at q11-q12

We report that a gene responsible for familial hypertrophic cardiomyopathy (HC) is closely linked to the cardiac alpha and beta myosin heavy chain (MHC) genes on chromosome 14q11. We have recently shown that probe CRI-L436, derived from the anonymous DNA locus D14S26, detects a polymorphic restriction fragment that segregates with familial HC in affected members of a large Canadian family. Using chromosomal in situ hybridization, we have mapped CRI-L436 to chromosome 14 at q11-q12. Because the cardiac MHC genes also map to this chromosomal band, we have determined the genetic distances between the cardiac beta MHC gene, D14S26, and the familial HC locus. Data presented here show that these three loci are linked within 5 centimorgans on chromosome 14 at q11-q12. The possibility that defects in either the cardiac alpha or beta MHC genes are responsible for familial HC is discussed.     

Attenuation of SARS‐CoV‐2 replication and associated inflammation by concomitant targeting of viral and host cap 2'‐O‐ribose methyltransferases

The SARS‐CoV‐2 infection cycle is a multistage process that relies on functional interactions between the host and the pathogen. Here, we repurposed antiviral drugs against both viral and host enzymes to pharmaceutically block methylation of the viral RNA 2''‐O‐ribose cap needed for viral immune escape. We find that the host cap 2''‐O‐ribose methyltransferase MTr1 can compensate for loss of viral NSP16 methyltransferase in facilitating virus replication. Concomitant inhibition of MTr1 and NSP16 efficiently suppresses SARS‐CoV‐2 replication. Using in silico target‐based drug screening, we identify a bispecific MTr1/NSP16 inhibitor with anti‐SARS‐CoV‐2 activity in vitro and in vivo but with unfavorable side effects. We further show antiviral activity of inhibitors that target independent stages of the host SAM cycle providing the methyltransferase co‐substrate. In particular, the adenosylhomocysteinase (AHCY) inhibitor DZNep is antiviral in in vitro, in ex vivo, and in a mouse infection model and synergizes with existing COVID‐19 treatments. Moreover, DZNep exhibits a strong immunomodulatory effect curbing infection‐induced hyperinflammation and reduces lung fibrosis markers ex vivo. Thus, multispecific and metabolic MTase inhibitors constitute yet unexplored treatment options against COVID‐19.