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The series publishes monographs and edited volumes that showcase significant scholarly work at the various intersections that currently motivate interdisciplinary inquiry in German cultural studies. Topics span German-speaking lands and cultures from the 18th to the 21st century, with a special focus on demonstrating how various disciplines and new theoretical and methodological paradigms work across disciplinary boundaries to create knowledge and add to critical understanding in German studies. The series editor is a renowned professor of German studies in the United States who penned one of the foundational texts for understanding what interdisciplinary German cultural studies can be. All works are peer-reviewed and in English. Three new titles will be published annually. About the series editor: Irene Kacandes is the Dartmouth Professor of German Studies and Comparative Literature at Dartmouth College, Hanover, New Hampshire. Shereceived three degrees from Harvard University and also studied at the Free University of Berlin and Aristotle University in Thessaloniki, Greece. She publishes on a wide range of interdisciplinary topics including secondary orality, rhetoric, aesthetics, trauma, witnessing, family and generational memory, experimental life writing, Holocaust testimony, and narrative theory. She has lectured widely in the United States and Europe and currently serves as President of the International Society for the Study of Narrative and Vice President of the German Studies Association.

The Routledge Companion to the Literature of the U.S. South provides a collection of vibrant and multidisciplinary essays by scholars from a wide range of backgrounds working in the field of U.S. Southern studies.

This thesis provides a detailed historical overview of the serial translations of fiction and non-fiction that appeared in the Hawaiian language newspapers between 1834 and 1895. Making up between 20% and 30% of the columns each day, week, or month, these translations provided Hawaiian readers with access to popular culture, historical information, and narrative entertainment drawn from European, American, and British book-length and serial publications, whether single volumes, magazines, or newspapers. When possible, this thesis identifies the source publications and their authors, as well the translators who produced Hawaiian versions. The narrative proceeds chronologically, providing information about the specific translations appearing in the many Hawaiian language newspapers published during this period, as well as about the duration of their serialization. In keeping with the studied materials, the thesis is written in Hawaiian.

Background: Periodontitis is a prevalent chronic inflammatory disease driven bydysbiotic subgingival microbial communities and characterized by progressive destruction of the periodontal attachment apparatus. Porphyromonas gingivalis functions as a keystone pathogen by systematically subverting Toll-like receptor (TLR) and complement-mediated innate immunity, sustaining tissue-destructive inflammation while evading bactericidal clearance. Sterile alpha and TIR motif-containing protein 1 (SARM1) is a TIR domain-containing adaptor and NAD+-cleaving enzyme that selectively suppresses TRIF-dependent interferon-β production and regulates macrophage inflammatory output through both adaptor and enzymatic functions. Despite the mechanistic convergence of SARM1 biology with the immune pathways manipulated by P. gingivalis, no study has directly investigated SARM1 in the context of periodontal tissue destruction.Objectives: This systematic review addressed three pre-specified research questions concerning the role of TIR adaptor proteins and SARM1 in innate immune responses to P. gingivalis, the molecular mechanisms of SARM1-mediated TLR regulation, and the preclinical and translational evidence supporting SARM1 as a therapeutic target in inflammatory and tissue-destructive disease contexts applicable to periodontitis.Methods: A systematic search of PubMed/MEDLINE, Scopus, Web of Science, and theCochrane Library was conducted without date restriction, supplemented by citation tracking of five anchor papers. Studies were selected according to pre-specified eligibility criteria encompassing any design addressing SARM1, TIR adaptor signaling, P. gingivalis innate immune evasion, periodontal bone loss, or SARM1-targeted therapeutic intervention. Data was extracted into a structured table and synthesized narratively given the heterogeneity of included study designs. The certainty of evidence was appraised using the GRADE framework across fourteen discrete outcomes. PROSPERO: CRD420261405547.Results: Sixty-nine unique primary studies were included across five thematic groups. All fourteen outcomes were rated Very Low certainty (⊕⊖⊖⊖) by GRADE appraisal, with indirectness — reflecting the complete absence of studies directly linking SARM1 to P. gingivalis infection or periodontal tissue — as the primary driver of downgrading. Key findings included: SARM1 selectively suppressed TRIF-dependent IFN-β without equivalent MyD88- dependent NF-κB suppression across four independent systems; SARM1 NADase activity was confirmed across six independent groups with cryo-EM structural resolution; SARM1 knockout in primary human monocytes increased IL-1β, TNF-α, and inflammasome activity through NADase-dependent and -independent mechanisms; P. gingivalis deploys gingipain-mediated MyD88 degradation, C5aR–TLR2 crosstalk, and complement subversion to uncouple inflammation from bactericidal immunity; and global Sarm1 knockout protected against diabetic bone disease in female mice through sustained osteoblast function and abrogation of oxidative stress responses, independent of neuropathy.Discussion: The evidence supports a coherent mechanistic proposition: SARM1's constitutive TRIF-specific suppression of IFN-β converges with and compounds the IFN-deficient immune environment engineered by P. gingivalis, while SARM1's potential NADase activation in the metabolically stressed periodontium (driven by CD38-mediated NAD+depletion, mitochondrial dysfunction, and inflammatory metabolic reprogramming) would further dysregulate macrophage inflammatory output, prime NLRP3 inflammasome activation, sustain AP-1-driven MMP transcription in stromal cells, and impair the pro-resolution macrophage phenotype switching required for periodontal repair. Pharmacological SARM1 NADase inhibitors have demonstrated in vivo efficacy across neuropathy and infection models, and TLR pathway inhibition consistently reduced alveolar bone loss across six independent animal intervention studies, validating the broader therapeutic principle.Conclusion: This review identifies SARM1 as a mechanistically plausible and pharmacologically accessible node in the immunopathology of chronic periodontitis that has not previously been investigated in this context. The Very Low certainty of the available evidence reflects a research frontier rather than poor study quality, and a targeted experimental program — including direct measurement of SARM1 activity in periodontal tissue, investigation of SARM1 function in P. gingivalis-infected macrophages, and evaluation of SARM1 NADase inhibitors in murine periodontitis models — is identified as the priority agenda for future research.