Post-surgical mental health appears to be highly relevant in terms of weight loss maintenance. It is likely that the surgical outcome could be positively influenced if patients at risk of developing mental health issues or eating disorders were identified and monitored in order to offer targeted interventions.

Bariatric surgery has serious implications on metabolic health. The reasons for a failure of bariatric surgery, i.e., limited weight loss, are multifactorial and include psychological factors. We established a theoretical model of how impulsivity is related to weight loss outcome. We propose that depressive symptoms act as a mediator between impulsivity and pathological eating behavior, and that pathological eating behavior has a direct impact on weight loss outcome. We calculated excessive weight loss (%EWL) and assessed self-reported impulsivity (using the Baratt Impulsiveness Scale (BIS-15) total score), depressive symptoms (the Patient Health Questionnaire (PHQ-9) score), and pathological eating behavior (the Eating Disorder Inventory 2 (EDI-2) total score) in 65 patients four years after laparoscopic sleeve gastrectomy. Regression and mediation analyses were computed to validate the theoretical model. The BIS-15, PHQ-9, and EDI-2 have medium to high correlations between each other, and EDI-2 correlated with %EWL. The mediation analysis yielded that the PHQ-9 represents a significant mediator between BIS-15 and EDI-2. The regression model between EDI-2 and %EWL was also significant. These results support our theoretical model, i.e., suggest that impulsivity has an indirect impact on weight loss outcome after bariatric surgery, mediated by depression and transferred through pathological eating behavior. Thus, the underlying psychological factors should be addressed in post-operative care to optimize weight loss outcome.

The limited hemocompatibility of currently used oxygenator membranes prevents long-term use of artificial lungs in patients with lung failure. To improve hemocompatibility, we developed a novel covalent C1-esterase inhibitor (C1-INH) coating. Besides complement inhibition, C1-INH also prevents FXII activation, a very early event of contact phase activation at the crossroads of coagulation and inflammation. Covalently coated heparin, as the current anticoagulation gold standard, served as control. Additionally, a combination of both coatings (C1-INH/heparin) was established. The coatings were tested for their hemocompatibility by dynamic incubation with freshly drawn human whole blood. The analysis of various blood and plasma parameters revealed that C1-INH-containing coatings were able to markedly reduce FXIIa activity compared to heparin coating. Combined C1-INH/heparin coatings yielded similarly low levels of thrombin-antithrombin III complex formation as heparin coating. In particular, adhesion of monocytes and platelets as well as the diminished formation of fibrin networks were observed for combined coatings. We could show for the first time that a covalent coating with complement inhibitor C1-INH was able to ameliorate hemocompatibility. Thus, the early inhibition of the coagulation cascade is likely to have far-reaching consequences for the other cross-reacting plasma protein pathways.

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