Speaking with a KN95 face mask: a within-subjects study on speaker adaptation and strategies to improve intelligibility.

Mask-wearing during the COVID-19 pandemic has prompted a growing interest in the functional impact of masks on speech and communication. Prior work has shown that masks dampen sound, impede visual communication cues, and reduce intelligibility. However, more work is needed to understand how speakers change their speech while wearing a mask and to identify strategies to overcome the impact of wearing a mask. Data were collected from 19 healthy adults during a single in-person session. We investigated the effects of wearing a KN95 mask on speech intelligibility, as judged by two speech-language pathologists, examined speech kinematics and acoustics associated with mask-wearing, and explored KN95 acoustic filtering. We then considered the efficacy of three speaking strategies to improve speech intelligibility: Loud, Clear, and Slow speech. To inform speaker strategy recommendations, we related findings to self-reported speaker effort. Results indicated that healthy speakers could compensate for the presence of a mask and achieve normal speech intelligibility. Additionally, we showed that speaking loudly or clearly-and, to a lesser extent, slowly-improved speech intelligibility. However, using these strategies may require increased physical and cognitive effort and should be used only when necessary. These results can inform recommendations for speakers wearing masks, particularly those with communication disorders (e.g., dysarthria) who may struggle to adapt to a mask but can respond to explicit instructions. Such recommendations may further help non-native speakers and those communicating in a noisy environment or with listeners with hearing loss.

SARS-CoV-2 Infection Induces Psoriatic Arthritis Flares and Enthesis Resident Plasmacytoid Dendritic Cell Type-1 Interferon Inhibition by JAK Antagonism Offer Novel Spondyloarthritis Pathogenesis Insights.

Objective: Bacterial and viral infectious triggers are linked to spondyloarthritis (SpA) including psoriatic arthritis (PsA) development, likely via dendritic cell activation. We investigated spinal entheseal plasmacytoid dendritic cells (pDCs) toll-like receptor (TLR)-7 and 9 activation and therapeutic modulation, including JAK inhibition. We also investigated if COVID-19 infection, a potent TLR-7 stimulator triggered PsA flares. Methods: Normal entheseal pDCs were characterized and stimulated with imiquimod and CpG oligodeoxynucleotides (ODN) to evaluate TNF and IFNα production. NanoString gene expression assay of total pDCs RNA was performed pre- and post- ODN stimulation. Pharmacological inhibition of induced IFNα protein was performed with Tofacitinib and PDE4 inhibition. The impact of SARS-CoV2 viral infection on PsA flares was evaluated. Results: CD45+HLA-DR+CD123+CD303+CD11c- entheseal pDCs were more numerous than blood pDCs (1.9 ± 0.8% vs 0.2 ± 0.07% of CD45+ cells, p=0.008) and showed inducible IFNα and TNF protein following ODN/imiquimod stimulation and were the sole entheseal IFNα producers. NanoString data identified 11 significantly upregulated differentially expressed genes (DEGs) including TNF in stimulated pDCs. Canonical pathway analysis revealed activation of dendritic cell maturation, NF-κB signaling, toll-like receptor signaling and JAK/STAT signaling pathways following ODN stimulation. Both tofacitinib and PDE4i strongly attenuated ODN induced IFNα. DAPSA scores elevations occurred in 18 PsA cases with SARS-CoV2 infection (9.7 ± 4 pre-infection and 35.3 ± 7.5 during infection). Conclusion: Entheseal pDCs link microbes to TNF/IFNα production. SARS-CoV-2 infection is associated with PsA Flares and JAK inhibition suppressed activated entheseal plasmacytoid dendritic Type-1 interferon responses as pointers towards a novel mechanism of PsA and SpA-related arthropathy.