Managing the "Three Cs" of Academic Literature Authorship: Contributions, Credit, and Conflict.

Dissemination of information through publications is central to academic research, as well as professional advancement. Although seemingly a straightforward endeavor, publication authorship may present challenges. Although the International Committee of Medical Journal Editors defines authorship based on 4 required criteria, contemporary interdisciplinary collaborations can complicate authorship determinations. However, communication that occurs early and frequently in the research and writing process can help to prevent or mitigate potential conflicts, while a process for defining authorship contributions can aid in awarding proper credit. The Contributor Roles Taxonomy (CRediT) defines 14 essential roles of manuscript authors that can be utilized to characterize individual author contributions toward any given publication. This information is useful for academic administrators when evaluating contributors of faculty during promotion and tenure decisions. In the era of collaborative scientific, clinical, and pedagogical scholarship, providing faculty development, including statements of credit in the published work, and developing institutional systems to capture and assess contributions are key.

Targeting NLRP3 signaling by a novel-designed sulfonylurea compound for inhibition of microglial inflammation.

The nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome plays an important role in microglia-mediated inflammation. Dysregulation of NLRP3 signaling results in microglial activation and triggers inflammatory responses contributing to the development of neurological disorders including ischemic stroke, schizophrenia, Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Inhibition of the NLRP3-linked inflammatory pathways reduces microglia-induced inflammation and is considered as a promising therapeutic approach for neuro-inflammatory diseases. In the present study, we report the development of AMS-17, a rationally-designed tertiary sulfonylurea compound for inhibition of inflammation in microglia. AMS-17 inhibited expression of the NLRP3, and its downstream components and cytokines such as caspase-1, tumor necrosis factor-α (TNF-α), IL-1ß and inducible nitric oxide synthase (iNOS). It also suppressed lipopolysaccharide (LPS)-induced N9 microglial cell phagocytosis in vitro and activation of the microglia in mouse brain in vivo. Together, these results provide promising evidences for the inhibitory effects of AMS-17 in inflammation. This proof-of-concept study provides a new chemical scaffold, designed with the aid of pharmacophore modeling, with NLRP3 inhibitory activity which can be further developed for the treatment of inflammation-associated neurological disorders.