Prevalence of adverse childhood experiences and effect on outcomes in bariatric surgery patients: a systematic review and meta-analysis.

Adverse childhood experiences (ACEs) are defined as childhood maltreatment (sexual, physical, and emotional abuse and neglect) and other childhood traumatic experiences. Published prevalence estimates for ACEs in bariatric samples vary greatly and evidence on the association between ACEs and bariatric surgery weight loss and psychosocial outcomes is inconclusive. A systematic literature search on PubMed/Medline, PsycInfo, Web of Science, CINAHL (Cumulative Index of Nursing and Allied Health Literature), and Open Grey for studies published until August 30, 2021, yielded 21 publications for qualitative synthesis: 20 reporting on prevalence of ACEs in bariatric surgery candidates and patients, and 10 on the association of ACEs with outcomes. In meta-analysis, overall moderate to high heterogeneity was observed for prevalence estimates and moderate heterogeneity was observed for associations. Prevalence estimate for at least 1 form of ACEs (6 studies, n = 1368 patients) was 51% (95% confidence interval [CI]: 32%-70%). Effect size (Hedge's g) for the difference between the groups of patients reporting any or a high number of ACEs versus no or a low number of ACEs was calculated from means, standard deviations and group size, or P values. Based on 7 studies (n = 946 patients), the association between ACEs and weight loss was not significant (Hedge's g = -.15 [95% CI: -.38 to .09]; I2 = 53%), regardless of short- or long-term follow-up (P = .413) and the proportion of patients in each study receiving Roux-en-Y gastric bypass (RYGB) (ß = .0005, P = .868). Preliminary findings based on 3 short- and long-term studies (n = 414 patients) showed that ACEs were significantly (P = .001) associated with higher postoperative depressive symptoms (Hedge's g = .50 [95% CI: .22-.78]; I2 = 36%). Associations between ACEs and other psychosocial outcomes such as eating pathology were reported narratively. There is a need for additional long-term studies using validated assessment tools for ACEs to evaluate the effect of ACEs on weight and psychosocial outcomes after bariatric surgery.

[Possibilities for Universities to Influence Global Pricing of Medicines]. / Möglichkeiten der universitären Einflussnahme auf die globale Preisgestaltung von Medikamenten.

People in countries of the global south are affected by a unique spectrum of diseases, while costs for health care are a huge burden in the context of poverty. Furthermore, non-communicable diseases increasingly play a role in these countries. The management of translational research, potential clinical applications and marketing of new drugs in Germany is thus getting more and more important for global health. Regarding this, universities have a particular responsibility for two reasons. First, through basic research, they contribute significantly to the development of new medicines. Second, the university is a public institution and has thus the responsibility to return the gained knowledge to the public. Marketing of publicly funded innovations should provide benefits to patients in wealthy and poor countries alike. As a first step towards this goal, we demand the introduction of a globally responsible licensing policy at German universities. Different mechanisms which have been described in the German speaking areas such as "Equitable Licensing" provide a basis for the realization of this ambitious aim and have been introduced successfully at the universities of Muenster, Tuebingen and Freiburg.

Deficiency of iPLA2ß Primes Immune Cells for Proinflammation: Potential Involvement in Age-Related Mesenteric Lymph Node Lymphoma.

Proinflammation can predispose the body to autoimmunity and cancer. We have reported that iPLA2ß(-/-) mice are susceptible to autoimmune hepatitis and colitis. Here we determined whether cytokine release by immune cells could be affected by iPLA2ß deficiency alone or combined with CD95/FasL-antibody treatment in vivo. We also determined whether cancer risk could be increased in aged mutant mice. Immune cells were isolated from 3-month old male WT and iPLA2ß(-/-) mice, and some were injected with anti-CD95/FasL antibody for 6 h. Kupffer cells (KC) or splenocytes and liver lymphocytes were stimulated in vitro by lipopolysaccharide or concanavalinA, respectively. Whole-body iPLA2ß deficiency caused increased apoptosis in liver, spleen, and mesenteric lymph node (MLN). KC from mutant mice showed suppressed release of TNFα and IL-6, while their splenocytes secreted increased levels of IFNγ and IL-17a. Upon CD95/FasL activation, the mutant KC in turn showed exaggerated cytokine release, this was accompanied by an increased release of IFNγ and IL-17a by liver lymphocytes. Aged iPLA2ß(-/-) mice did not show follicular MLN lymphoma commonly seen in aged C57/BL6 mice. Thus, iPLA2ß deficiency renders M1- and Th1/Th17-proinflammation potentially leading to a reduction in age-related MLN lymphoma during aging.

Deficiency of Group VIA Phospholipase A2 (iPLA2ß) Renders Susceptibility for Chemical-Induced Colitis.

BACKGROUND: Inflammatory bowel disease results from a combination of dysfunction of intestinal epithelial barrier and dysregulation of mucosal immune system. iPLA2ß has multiple homeostatic functions and shown to play a role in membrane remodeling, cell proliferation, monocyte chemotaxis, and apoptosis. The latter may render chronic inflammation and susceptibility for acute injury. AIMS: We aim to evaluate whether an inactivation of iPLA2ß would enhance the pathogenesis of experimental colitis induced by dextran sodium sulfate. METHODS: iPLA2ß-null male mice were administered dextran sodium sulfate in drinking water for 7 days followed by normal water for 3 days. At day 10, mice were killed, and harvested colon and ileum were subjected for evaluation by histology, immunohistochemistry, and quantitative RT-PCR. RESULTS: Dextran sodium sulfate administration caused a significant increase in histological scores and cleaved caspase 3 (+) apoptosis concomitant with a decrease in colon length and crypt cell Ki67 (+) proliferation in iPLA2ß-null mice in a greater extent than in control littermates. This sensitization by iPLA2ß deficiency was associated with an increase in accumulation of F4/80 (+) macrophages, and expression of proinflammatory cytokines and chemokines, while the number of mucin-containing goblet cells and mucus layer thickness was decreased. Some of these abnormalities were also observed in the ileum. CONCLUSIONS: An inactivation of iPLA2ß exacerbated pathogenesis of experimental colitis by promoting intestinal epithelial cell apoptosis, inhibiting crypt cell regeneration, and causing damage to mucus barrier allowing an activation of innate immune response. Thus, iPLA2ß may represent a susceptible gene for the development of inflammatory bowel disease.