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This article considers how Marianne Hirsch's concept of postmemory is applicable to the grandchildren of Holocaust survivors by analyzing two graphic novels: Rutu Modan's The Property and Amy Kurzweil's Flying Couch. Postmemory emerged as a theory for understanding how traumatic memories become inherited by survivors' children. Both texts show that while the children of the survivors are burdened by their parents' memories, this is not the case for the grandchildren. Instead, it is only in the third generation that postmemories are liberated from being exclusively memories of trauma, and as a result, new approaches to the Holocaust emerge.

Amy Kurzweil’s graphic memoir Flying Couch demonstrates the lingering struggles the third generation of Holocaust survivors face in trying to understand their own identities. This article examines Flying Couch and Kurzweil’s struggles with her familial Holocaust trauma. Through the use of maps, Kurzweil examines her relationship to her grandmother, a Holocaust survivor, and her mother, a member of the second generation after the Holocaust. The article argues that while these maps work to ground both Kurzweil and the narrative itself, these attempts actually emphasize the instability with which Kurzweil still grapples. However, Kurzweil’s inclusion of various forms of mapping consists of more than recognizing her grandmother’s Holocaust trauma because she also examines her relationship to her mother, and her own identity as an individual. These maps create opportunities in which she can understand her identity as a part of and apart from her familial trauma. Through these familial interactions, the maps in Flying Couch create a generational topography in which they serve two important functions: (1) to connect Kurzweil with her familial and intergenerational Holocaust trauma, and (2) to allow Kurzweil to understand her sense of self apart from this intergenerational trauma.

The bacteria inhabiting the mammalian gastrointestinal (GI) tract play a vital role in normal digestion and immune function. In a healthy host, the immune system is tolerant to gut bacteria and does not mount an effector response to bacteria-derived antigens. Loss of tolerance to intestinal microflora has been associated with inflammatory bowel disease (IBD) in both mice and humans. Mice lacking Ndfip1, an adaptor protein for E3 ubiquitin ligases of the Nedd4-family, in T cells (Ndfip1-cKO) develop a disease resembling IBD. Inflammation in these mice is characterized by increased activation of peripheral T cells, infiltration of eosinophils into the GI tract, and epithelial hypertrophy in the esophagus. We hypothesized that this intestinal inflammation in Ndfip1-cKO mice is caused by a loss of T-cell tolerance to bacterial antigens. Here, we show that treatment of Ndfip1-cKO mice with broad-spectrum antibiotics drastically reduced bacterial load in stool but had little effect on T-cell activation and did not affect eosinophil infiltration into the GI tract or epithelial hypertrophy in the esophagus. Thus, inflammation in Ndfip1-cKO mice is not caused by a loss of tolerance to intestinal microbiota. Rather, T cell activation and eosinophilia may instead be triggered by other environmental antigens.