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Transmutation detectors (TMDs) are based on a similar principle as neutron activation detectors (NADs). In both cases, the neutron fluence is estimated from the number of reactions in the detectors. The main differences between these two detectors are the type of product created by the nuclear reaction and the evaluation of the irradiated detectors. In TMD, the transmuted nuclide is stable, and the number of reactions is gained by analytical methods suitable for measuring low concentrations. In NAD, the nuclear reaction leads to the production of radionuclides and the number of reactions is evaluated from the activity measured by radiometric instruments. While TMDs for thermal neutrons can be easily prepared and evaluated due to their high thermal neutron cross sections for isotopes such as 10B, 115In or 197Au, the requirements for fast neutron TMDs are higher. Cross sections for nuclear reactions suitable for the TMD method with fast neutrons are in the range of 1 to 100 mb for the fission spectrum. This leads to concentrations from 0.01 ppm to 1 ppm for fast neutron fluence of 1E19 cm-2. These low concentrations imply requirements for detector material purity and sensitivity of concentration evaluation equipment. Materials for fast neutron TMDs were proposed, where the relevant parameters, such as energy threshold and minimal detectable fluence are known and convenient. An experimental comparison of some TMD and NAD responses was made in the LVR-15 research reactor using secondary ion mass spectrometry to evaluate the concentration of TMDs.

On September 26th, 2022, the detonations at the gas pipelines Nord Stream 1 and 2 resulted in some of the largest non-natural releases of methane known. The distribution of methane in the surrounding seawater and the possible effects were not apparent. To trace the pathways of methane we recorded CH 4 concentrations and the isotopic signal (δ 13 C-CH 4 ) in seawater, and air. A week post-explosion, we detected methane concentrations up to 4 orders of magnitude above the natural Baltic Sea background. The released fossil methane created a distinct plume with δ 13 C-CH 4 ratios differing from natural background values. The strong water stratification preserved the distribution pattern initiated by the explosion, shown by the laterally strong concentration gradient within the plume. Our analysis encompasses three stages of the explosion's impact; the initial sea-air methane release, measurements taken during our research expedition one week later, and a third stage triggered by the shift from summer to winter conditions as an outlook on how winter mixing and microbial activity will influence the plume., (© 2024. The Author(s).)

Dysregulation of the BCL-2 family is implicated in protecting chronic myeloid leukemia (CML) cells from intracellular damage and BCR::ABL1-inhibition with tyrosine kinase inhibitors (TKIs) and may be a viable therapeutic target in blast phase (BP-)CML, for which treatment options are limited. BH3 mimetics, a class of small molecule inhibitors with high-specificity against the prosurvival members of the BCL-2 family, have displayed clinical promise in the treatment of chronic lymphocytic and acute myeloid leukemia as single agents and in combination with standard-of-care therapies. Here we present the first comparison of inhibition of BCL-2 prosurvival proteins BCL-2, BCL-xL and MCL-1 in combination with a second or third generation TKI, crucially with comparisons drawn between myeloid and lymphoid BP-CML samples. Co-treatment of four BP-CML cell lines with the TKIs nilotinib or ponatinib and either BCL-2 (venetoclax), MCL-1 (S63845) or BCL-xL (A-1331852) inhibitors resulted in a synergistic reduction in cell viability and increase in phosphatidylserine (PS) presentation. Nilotinib with BH3 mimetic combinations in myeloid BP-CML patient samples triggered increased induction of apoptosis over nilotinib alone, and a reduction in colony-forming capacity and CD34 + fraction, while this was not the case for lymphoid BP-CML samples tested. While some heterogeneity in apoptotic response was observed between cell lines and BP-CML patient samples, the combination of BCL-xL and BCR::ABL1 inhibition was consistently effective in inducing substantial apoptosis. Further, while BH3 mimetics showed little efficacy as single agents, dual-inhibition of BCL-2 prosurvival proteins dramatically induced apoptosis in all cell lines tested and in myeloid BP-CML patient samples compared to healthy donor samples. Gene expression and protein level analysis suggests a protective upregulation of alternative BCL-2 prosurvival proteins in response to BH3 mimetic single-treatment in BP-CML. Our results suggest that BH3 mimetics represent an interesting avenue for further exploration in myeloid BP-CML, for which alternative treatment options are desperately sought., (© 2022. The Author(s).)