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Despite the energy penalty and solvent regeneration cost, carbon capture using amine-based absorption/stripping systems is one of the most used technologies for CO2 removal of post-combustion processes, mainly due to its high capture efficiency. This work presents a complex control strategy for a post-combustion carbon capture plant that aims to minimize the effect of disturbances and maintain the desired performance of the CO2 capture system. It is based on a comprehensive mathematical model for the plant considered to have, in addition to the absorption/stripping columns, a buffer tank and heat exchangers designed to ensure energy efficiency and to determine the flexible, smooth, and robust operation of the plant. The buffer tank is provided with 3 control loops that have the purpose of adjusting the parameters of the absorber inlet solvent solution, such as downstream disturbances that are, to a less extent, recirculated back into the system from the desorber. Using a model predictive control algorithm, an additional control system was designed with the aim to maintain the carbon capture rate of the plant at the setpoint value of 85 % and to keep the reboiler liquid temperature at 395 K setpoint. The control performance results are shown for the hybrid control approach that includes the MPC controller. Results show that the control approach can simultaneously control the targeted variables while efficiently coping with the intrinsic and complex input-output interactions. It is able to maintain better the controlled variables at the desired setpoint values, despite the typical flowrate and concentration disturbances of the CO2 influent flue gas flow. This is achieved with reduced offset and minimal peak deviations from the setpoints. The mean absolute error values of the controllers are maintained below 7 %, and the carbon capture rate is maintained above 78 % at all times. The energy performance index is maintained at values below 3.5 MJ/kgCO2. [ABSTRACT FROM AUTHOR]

We present the case of a 33-year-old male patient diagnosed with chronic phase chronic myeloid leukaemia in June 2008. According to treatment protocols enforced at that time, the patient started oral treatment with imatinib 400 mg/day, reaching a major molecular response (MMR) in 18-month time. The molecular response improved over the time, with an undetectable BCR-ABL1 transcript level after 36 -48 months of treatment. However, the profound molecular response did not last, requiring a switch to the second line of therapy after 75 months of imatinib. Taking nilotinib 400 mg x2/day, the patient achieved a major molecular response in 12 months, and after 18 months of treatment the level of BCR-ABL1 became undetectable. However, two vasooclusive events occurred in 2018 - a transient left parietal ischemic stroke and a left femoral artery occlusion - and in accordance with ESMO 2017 recommendations, nilotinib treatment was interrupted. The treatment free remission decision was made with monthly monitoring of the BCR-ABL1 transcript level, but since the 4th month of monitoring, the deep molecular response disappeared. Administration of dasatinib, the third tyrosine kinase inhibitor, resulted in a deep molecular response which currently lasted until now, during the 58 months of treatment. The presented case represents the evolution of the concept of treatment in this haemato-oncological disease during the last decade. [ABSTRACT FROM AUTHOR]

The epidermal growth factor receptor (EGFR) is highly expressed in gastric cancer indicating its suitability as a target for receptor tyrosine kinase (RTK) inhibitors. In the current study we explored the role of EGFR and its potential use as a therapeutic target in gastric cancer. First we analyzed 66 gastric cancer samples of Asian and Caucasian patients for the presence of EGFR mutations. No activating EGFR mutations were found and gefitinib alone was only weakly effective in gastric cancer cell lines. However, acetylsalicylic acid (ASA) significantly enhanced the inhibitory effects of gefitinib indicating synergistic action. Whole genome expression profiling indicated significant regulation of 120 genes in the case of co-administration of gefitinib and ASA (32 induced, 88 repressed) in gastric adenocarcinoma cells. Further analyses indicated that several important signalling pathways were effectively inhibited by simultaneous exposure to gefitinib and ASA. Our findings indicate that although gastric cancer does not seem to harbour mutations which render the cancer cells constitutively susceptible to gefitinib, the co-administration of ASA can strengthen RTK inhibitor activity in adenocarcinoma cells by EGFR activation. This is the first report of effective modulation of EGFR-inhibition activity in cancer.