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INTRODUCTION: COVID-19 causes a considerable degradation of pulmonary function to the point of an acute respiratory distress syndrome (ARDS). Over the course of the disease the gas exchange capability of the lung can get impaired to such an extent that extracorporeal membrane oxygenation (ECMO) is needed as a life-saving intervention. In patients COVID-19 as well as ECMO may cause severe coagulopathies which manifest themselves in micro and macro thrombosis. Previous studies established D-dimers as a marker for critical thrombosis of the ECMO system while on admission increased D-dimers are associated with a higher mortality in COIVD-19 patients. It is therefore crucial to determine if COVID-19 poses an increased risk of early thrombosis of the vital ECMO system. METHODS: 40 patients who required ECMO support were enrolled in a retrospective analysis and assigned into 2 groups. The COVID group consist of 20 COVID-19 patients who required ECMO support (n = 20), whereas 20 ECMO patients without COVID-19 were assigned to the control group. D-dimers, fibrinogen, antithrombin III (AT III), lactate dehydrogenase (LDH) and platelet count were analysed using locally weighted scatterplot smoothing and MANOVAs. RESULTS: The analysis of both groups shows highly significant differences in the dynamics of hemostasis. The increase in D-dimers that is associated with thrombosis of the ECMO systems occurs in COVID-19 patients around 2 days earlier (p = 2,8115 10–11) while fibrinogen is consumed steadily. In the control group fibrinogen levels increase rapidly after ten days with a plateau phase of around five days (p = 1,407 10–3) . Both groups experience a rapid increase in AT III after start of support by ECMO (p = 5,96 10–15). In the COVID group platelet count decreased from 210 giga/l to 130 giga/l within eight days, while in the same time span in the control group platelets decreased from 180 giga/l to 105 giga/l (p = 1,1 10–15). In both groups a marked increase in LDH beyond 5000 U/l occurs (p = 3,0865 10–15). CONCLUSION: The early increase in D-dimers and decrease in fibrinogen suggests that COVID-19 patients bear an increased risk of early thrombosis of the ECMO system compared to other diseases treated with ECMO. Additionally, the control group shows signs of severe inflammation 10 days after the start of ECMO which were absent in COVID-19 patients. [ABSTRACT FROM AUTHOR]

INTRODUCTION: COVID-19 causes a considerable degradation of pulmonary function to the point of an acute respiratory distress syndrome (ARDS). Over the course of the disease the gas exchange capability of the lung can get impaired to such an extent that extracorporeal membrane oxygenation (ECMO) is needed as a life-saving intervention. In patients COVID-19 as well as ECMO may cause severe coagulopathies which manifest themselves in micro and macro thrombosis. Previous studies established D-dimers as a marker for critical thrombosis of the ECMO system while on admission increased D-dimers are associated with a higher mortality in COIVD-19 patients. It is therefore crucial to determine if COVID-19 poses an increased risk of early thrombosis of the vital ECMO system. METHODS: 40 patients who required ECMO support were enrolled in a retrospective analysis and assigned into 2 groups. The COVID group consist of 20 COVID-19 patients who required ECMO support (n = 20), whereas 20 ECMO patients without COVID-19 were assigned to the control group. D-dimers, fibrinogen, antithrombin III (AT III), lactate dehydrogenase (LDH) and platelet count were analysed using locally weighted scatterplot smoothing and MANOVAs. RESULTS: The analysis of both groups shows highly significant differences in the dynamics of hemostasis. The increase in D-dimers that is associated with thrombosis of the ECMO systems occurs in COVID-19 patients around 2 days earlier (p = 2,8115 10–11) while fibrinogen is consumed steadily. In the control group fibrinogen levels increase rapidly after ten days with a plateau phase of around five days (p = 1,407 10–3) . Both groups experience a rapid increase in AT III after start of support by ECMO (p = 5,96 10–15). In the COVID group platelet count decreased from 210 giga/l to 130 giga/l within eight days, while in the same time span in the control group platelets decreased from 180 giga/l to 105 giga/l (p = 1,1 10–15). In both groups a marked increase in LDH beyond 5000 U/l occurs (p = 3,0865 10–15). CONCLUSION: The early increase in D-dimers and decrease in fibrinogen suggests that COVID-19 patients bear an increased risk of early thrombosis of the ECMO system compared to other diseases treated with ECMO. Additionally, the control group shows signs of severe inflammation 10 days after the start of ECMO which were absent in COVID-19 patients. [ABSTRACT FROM AUTHOR]

The nitrogen phosphotransferase system (PTSNtr) of Pseudomonas putida is a multi-component regulatory device that participates in controlling a variety of physiological processes in a post-translational fashion. A general survey of genes regulated by PtsN exposed transcription of the kdpFABC operon is most conspicuously affected. Measurements of kdpFp promoter activity in different pts mutants showed that PtsN is responsible for repression of kdpFABC transcription. This effect could be assigned mainly to PtsN~P, depending on the external K+ concentration. Bacterial two-hybrid assays demonstrated that kdpFp regulation is implemented through direct interaction of the PtsN protein with the sensor kinase KdpD of the KdpD/KdpE two-component system. Interaction between KdpD and PtsN was detectable with a PtsN variant that imitates the non-phosphorylated form as well as with a PtsN type mimicking the phosphorylated form of PtsN. These results raise a regulatory scenario in which the Kdp system is regulated by the action of PtsN through direct interaction with the sensor kinase KdpD, and the outcome of such an interaction depends on the phosphorylation state of PtsN as well as on the external K+ concentration. [ABSTRACT FROM AUTHOR]