8 research outputs found

    Changes in primary and secondary hemostasis in patients with CLL treated with venetoclax and ibrutinib

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    Bleeding is a common adverse event following ibrutinib monotherapy. However, it remains unclear how hemostasis is affected by venetoclax in combination with ibrutinib. Here we investigated hemostasis in patients with chronic lymphocytic leukemia (CLL) at baseline, during ibrutinib monotherapy, and during venetoclax and ibrutinib combination therapy or venetoclax monotherapy. Primary hemostasis, assessed by Multiplate using adenosine diphosphate (ADP), arachidonic acid (AA), and thrombin receptor agonist peptide (TRAP-6), was impaired in all CLL patients at baseline, remained unchanged upon ibrutinib monotherapy, and improved significantly following venetoclax added to ibrutinib or as monotherapy. Secondary hemostasis assessed by thromboelastography (TEG) was normal and unchanged throughout treatment. The frequency of clinical bleeding events was the highest during ibrutinib monotherapy, in line with the demonstrated improved primary hemostasis upon addition of venetoclax, thus pointing toward a treatment option for CLL patients with increased bleeding risk

    Increased CO2 evolution caused by heat treatment in wood-decaying fungi

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    Wood-decaying fungi are regarded as the main decomposers of woody debris in boreal forests. Given that fungal respiration makes a significant contribution to terrestrial carbon flows, it is important to understand how the wood-decaying fungal metabolism is regulated in relation to different environmental conditions and disturbances. In the present study, we investigated the effect of temperature stress on wood decomposition rate in 18 species of wood-decaying fungi, representing a broad range of species-habitat associations. Heat shock duration and temperature were calibrated to match the conditions of a forest fire. We found a general increase in fungal decay rate after heat shock; the response was more pronounced in species associated with fire-prone forests. The underlying mechanism is unclear, but possibly relates to an up-regulation at the cellular level in response to heat shock. Our results show that the decomposition rate of dead wood can be strongly affected by environmental triggers
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