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Creep resistant 9% Cr steels are frequently used in civil engineering projects of supercritical coal‐fired power plants operating at temperatures of superheated steam around 610 °C. This work focus on analysis of microstructure degradation and degradation of mechanical properties of orbital narrow‐gap welding of P91 and P92 steels. Nowadays welding technology of orbital narrow‐gap using tungsten inert gas is not limited to welding of high‐pressure steam pipelines. This method is highly productive and efficient and leads to an increase in productivity, quality, and repeatability of welding process. It replaces the original method of manual welding with coated electrode into a standard bevel, which is a time‐consuming process that costs a high amount of weld metal. Welds are degraded at 650 °C/30 000 h without applied stress and the effect of degradation is evaluated across the weld based on the observed changes in microstructure and hardness. Attention is focused mainly on precipitation and coarsening of Laves phase in the main areas of heat affected zone (HAZ): coarse grain HAZ, fine grain HAZ, and intercritical HAZ. The results show that frequency and rate of Laves phase coarsening in the fine grain and coarse grain HAZ are higher than in the base material. [ABSTRACT FROM AUTHOR]

Understanding the molecular pathogenesis of MLL fusion oncoprotein (MLL-FP) leukaemia has spawned epigenetic therapies that have improved clinical outcomes in this often-incurable disease. Using genetic and pharmacological approaches, we define the individual and combined contribution of KAT6A, KAT6B and KAT7, in MLL-FP leukaemia. Whilst inhibition of KAT6A/B is efficacious in some pre-clinical models, simultaneous targeting of KAT7, with the novel inhibitor PF-9363, increases the therapeutic efficacy. KAT7 interacts with Menin and the MLL complex and is co-localised at chromatin to co-regulate the MLL-FP transcriptional program. Inhibition of KAT6/KAT7 provides an orthogonal route to targeting Menin to disable the transcriptional activity of MLL-FP. Consequently, combined inhibition rapidly evicts the MLL-FP from chromatin, potently represses oncogenic transcription and overcomes primary resistance to Menin inhibitors. Moreover, PF-9363 or genetic depletion of KAT7 can also overcome acquired genetic/non-genetic resistance to Menin inhibition. These data provide the molecular rationale for rapid clinical translation of combination therapy in MLL-FP leukaemia.