Objective Eating disorders (EDs) are complex, heterogeneous, and severe psychiatric syndromes. They are highly comorbid with obsessive–compulsive disorder (OCD) which exacerbates the course of illness and impedes treatment. However, the direct functional relations between EDs and OCD symptoms remain largely unexplored. Hence, using network analysis, we investigated the relationship between ED and OCD at the level of symptoms in a heterogeneous clinical sample. Method We used cross sectional data of 303 treatment‐seeking patients with clinically relevant ED and OCD pathology. We constructed a regularized partial correlation network that featured both ED and OCD symptoms as nodes. To determine each symptom's influence, we calculated expected influence (EI) as an index of symptom centrality (i.e., “importance”). Bridge symptoms (i.e., symptoms from one syndromic cluster that have strong connections to symptoms of another syndromic cluster) were identified by computing bridge expected influence metrics. Results Fear of weight gain and dietary restraint were especially important among the ED symptoms. Interference due to obsessions was the key feature of OCD. ED and OCD clustered distinctly with few potential bridges between clusters. Discussion This study underscores the importance of cognitive symptoms for both ED and OCD although direct functional links between the two clusters are missing. Potentially, a network incorporating nodes capturing features of personality may account for diagnostic comorbidity better than specific symptoms of EDs or features of OCD do.

Background Negative illness representations such as self-blame impede treatment-seeking behavior and therapy motivation in individuals with eating disorders (EDs). However, only one study so far has investigated how different explanatory models influence these beliefs in EDs. We aimed to expand these findings by introducing an explanatory model based on network theory (NT). Methods We presented three explanatory models to a diverse web-recruited sample (n = 290, 141 females, 149 males) with clinically elevated ED symptomatology. Participants either watched a video with a biological-genetic (BG), cognitive-behavioral (CB) or an NT explanatory model and were asked about illness representations before and after watching the video. Results The BG group showed significantly greater reductions in self-blame but a significant decrease in personal control and less optimistic expectation regarding timeline compared to the CB and NT groups. There were no group differences regarding the perception of the clinician, comprehensibility of the explanatory model and credibility of a CBT intervention. Conclusions Given the increasing popularity of biological-genetic explanatory models of EDs, it is important to note the disadvantages we found to be associated with these models. Our findings indicate that explanatory models emphasizing cognitive-behavioral (CB) principles and/or network theoretical (NT) underpinnings of EDs may serve to promote optimism and greater perceptions of personal agency in affected populations. This trial's registration number is 316.

Lysostaphin, a staphylococcus-derived staphylocidal substance, has widely been used in assays of granulocyte phagocytic and bactericidal capability. It rapidly kills extracellular bacteria. Thus, a separate determination of intracellular surviving bacteria can be performed. One prerequisite for this approach is the safe inactivation of lysostaphin (usually brought about by trypsin) before the intracellular bacteria are externalized for plating. This inactivation has been found by others to be incomplete. Data are presented demonstrating a safe inactivation of lysostaphin by trypsin, if the pH value is maintained within the alkaline range. A low variation of results is obtained by plotting the total number of bacteria killed per incubate vs the logarithm of initial bacterial inoculum or of the intracellular surviving bacteria, leading to linear regression lines. The variation of the results increases greatly for initial bacteria/granulocyte proportions of greater than 5/1. The results obtained for two different St. aureus strains are significantly different. Dexamethasone pretreatment (12 mg p.o. within 8 h) had no detectable influence, when fresh blood was assayed, while blood storage at room temperature for 12 h (without dexamethasone pretreatment) led to a significant functional impairment, mainly of bactericidal capability when analyzed in a pairwise fashion. A major limitation of this kind of assays is that killed bacteria cannot be determined directly.

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