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The EU project HiPowAR studies a novel power generation system based on ammonia flameless oxidation with pure oxygen in a high-pressure membrane reactor and expansion of the resulting high-temperature H2O-N2 stream. The system combines the advantages of high temperature at expander inlet, typical of gas turbines, and small compression demand, typical of steam cycles. Water is injected into the reactor to control the very high adiabatic temperature, at the limited energy expenditure of liquid pumping. This work assesses the performance potential of the HiPowAR system under different design conditions, through simulations with a model developed in Aspen Plus®. The system shows a high efficiency (up to 55%) when operating at high temperature (e.g., 1350°C at expander inlet); hence, O2 membranes capable of working at very high temperature are required. The cycle features an optimal sub-atmospheric expansion pressure (in the range 0.1-0.2 bar), which requires the re-pressurization of the off-gas (steam-saturated nitrogen). The system also produces liquid water as a net output. A reduction of the expander inlet temperature to values acceptable by typical steam cycles (600°C) significantly limits the efficiency, despite allowing to demonstrate the process using conventional steam expanders.

In herpes simplex virus 1 (HSV-1), binding clusters enriched in CTCF during latency have been previously identified. We hypothesized that CTCF binding to CTCF clusters in HSV-1 would be disrupted in a reactivation event. To investigate, CTCF occupation of three CTCF binding clusters in HSV-1 was analyzed following sodium butyrate (NaB)- and explant-induced reactivation in the mouse. Our data show that the CTCF domains positioned within the HSV-1 genome, specifically around the latency-associated transcript (LAT) and ICP0 and ICP4 regions of the genome, lose CTCF occupancy following the application of reactivation stimuli in wild-type virus. We also found that CTCF binding clusters upstream of the ICP0 and ICP4 promoters both function as classical insulators capable of acting as enhancer blockers of the LAT enhancer. Finally, our results suggest that CTCF occupation of domains in HSV-1 may be differentially regulated both during latency and at early times following reactivation by the presence of lytic transcripts and further implicate epigenetic regulation of HSV-1 as a critical component of the latency-reactivation transition.