Improving readability and comprehension levels of otolaryngology patient education materials using ChatGPT.

OBJECTIVE: A publicly available large language learning model platform may help determine current readability levels of otolaryngology patient education materials, as well as translate these materials to the recommended 6th-grade and 8th-grade reading levels. STUDY DESIGN: Cross-sectional analysis. SETTING: Online using large language learning model, ChatGPT. METHODS: The Patient Education pages of the American Laryngological Association (ALA) and American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) websites were accessed. Materials were input into ChatGPT (OpenAI, San Francisco, CA; version 3.5) and Microsoft Word (Microsoft, Redmond, WA; version 16.74). Programs calculated Flesch Reading Ease (FRE) scores, with higher scores indicating easier readability, and Flesch-Kincaid (FK) grade levels, estimating U.S. grade level required to understand text. ChatGPT was prompted to "translate to a 5th-grade reading level" and provide new scores. Scores were compared for statistical differences, as well as differences between ChatGPT and Word gradings. RESULTS: Patient education materials were reviewed and 37 ALA and 72 AAO-HNS topics were translated. Overall FRE scores and FK grades demonstrated significant improvements following translation of materials, as scored by ChatGPT (p < 0.001). Word also scored significant improvements in FRE and FK following translation by ChatGPT for AAO-HNS materials overall (p < 0.001) but not for individual topics or for subspecialty-specific categories. Compared with Word, ChatGPT significantly exaggerated the change in FRE grades and FK scores (p < 0.001). CONCLUSION: Otolaryngology patient education materials were found to be written at higher reading levels than recommended. Artificial intelligence may prove to be a useful resource to simplify content to make it more accessible to patients.

Persistent post-COVID-19 smell loss is associated with immune cell infiltration and altered gene expression in olfactory epithelium.

SARS-CoV-2 causes profound changes in the sense of smell, including total smell loss. Although these alterations are often transient, many patients with COVID-19 exhibit olfactory dysfunction that lasts months to years. Although animal and human autopsy studies have suggested mechanisms driving acute anosmia, it remains unclear how SARS-CoV-2 causes persistent smell loss in a subset of patients. To address this question, we analyzed olfactory epithelial samples collected from 24 biopsies, including from nine patients with objectively quantified long-term smell loss after COVID-19. This biopsy-based approach revealed a diffuse infiltrate of T cells expressing interferon-γ and a shift in myeloid cell population composition, including enrichment of CD207+ dendritic cells and depletion of anti-inflammatory M2 macrophages. Despite the absence of detectable SARS-CoV-2 RNA or protein, gene expression in the barrier supporting cells of the olfactory epithelium, termed sustentacular cells, appeared to reflect a response to ongoing inflammatory signaling, which was accompanied by a reduction in the number of olfactory sensory neurons relative to olfactory epithelial sustentacular cells. These findings indicate that T cell-mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post-COVID-19 smell loss.

Persistent post-COVID-19 smell loss is associated with inflammatory infiltration and altered olfactory epithelial gene expression.

Most human subjects infected by SARS-CoV-2 report an acute alteration in their sense of smell, and more than 25% of COVID patients report lasting olfactory dysfunction. While animal studies and human autopsy tissues have suggested mechanisms underlying acute loss of smell, the pathophysiology that underlies persistent smell loss remains unclear. Here we combine objective measurements of smell loss in patients suffering from post-acute sequelae of SARS-CoV-2 infection (PASC) with single cell sequencing and histology of the olfactory epithelium (OE). This approach reveals that the OE of patients with persistent smell loss harbors a diffuse infiltrate of T cells expressing interferon-gamma; gene expression in sustentacular cells appears to reflect a response to inflammatory signaling, which is accompanied by a reduction in the number of olfactory sensory neurons relative to support cells. These data identify a persistent epithelial inflammatory process associated with PASC, and suggests mechanisms through which this T cell-mediated inflammation alters the sense of smell.

Aging-related olfactory loss is associated with olfactory stem cell transcriptional alterations in humans.

BACKGROUNDPresbyosmia, or aging-related olfactory loss, occurs in a majority of humans over age 65 years, yet remains poorly understood, with no specific treatment options. The olfactory epithelium (OE) is the peripheral organ for olfaction and is subject to acquired damage, suggesting a likely site of pathology in aging. Adult stem cells reconstitute the neuroepithelium in response to cell loss under normal conditions. In aged OE, patches of respiratory-like metaplasia have been observed histologically, consistent with a failure in normal neuroepithelial homeostasis.MethodsAccordingly, we have focused on identifying cellular and molecular changes in presbyosmic OE. The study combined psychophysical testing with olfactory mucosa biopsy analysis, single-cell RNA-Sequencing (scRNA-Seq), and culture studies.ResultsWe identified evidence for inflammation-associated changes in the OE stem cells of presbyosmic patients. The presbyosmic basal stem cells exhibited increased expression of genes involved in response to cytokines or stress or the regulation of proliferation and differentiation. Using a culture model, we found that cytokine exposure drove increased TP63, a transcription factor acting to prevent OE stem cell differentiation.ConclusionsOur data suggest aging-related inflammatory changes in OE stem cells may contribute to presbyosmia via the disruption of normal epithelial homeostasis. OE stem cells may represent a therapeutic target for restoration of olfaction.FundingNIH grants DC018371, NS121067, DC016224; Office of Physician-Scientist Development, Burroughs-Wellcome Fund Research Fellowship for Medical Students Award, Duke University School of Medicine.