Virtual Urgent Care Quality and Safety in the Time of Coronavirus.

BACKGROUND: Telemedicine use rapidly increased during the COVID-19 pandemic. This study assessed quality aspects of rapid expansion of a virtual urgent care (VUC) telehealth system and the effects of a secondary telephonic screening initiative during the pandemic. METHODS: A retrospective cohort analysis was performed in a single health care network of VUC patients from March 1, 2020, through April 20, 2020. Researchers abstracted demographic data, comorbidities, VUC return visits, emergency department (ED) referrals and ED visits, dispositions, intubations, and deaths. The team also reviewed incomplete visits. For comparison, the study evaluated outcomes of non-admission dispositions from the ED: return visits with and without admission and deaths. We separately analyzed the effects of enhanced callback system targeting higher-risk patients with COVID-like illness during the last two weeks of the study period. RESULTS: A total of 18,278 unique adult patients completed 22,413 VUC visits. Separately, 718 patient-scheduled visits were incomplete; the majority were no-shows. The study found that 50.9% of all patients and 74.1% of patients aged 60 years or older had comorbidities. Of VUC visits, 6.8% had a subsequent VUC encounter within 72 hours; 1.8% had a subsequent ED visit. Of patients with enhanced follow-up, 4.3% were referred for ED evaluation. Mortality was 0.20% overall; 0.21% initially and 0.16% with enhanced follow-up (p = 0.59). Males and black patients were significantly overrepresented in decedents. CONCLUSION: Appropriately deployed VUC services can provide a pragmatic strategy to care for large numbers of patients. Ongoing surveillance of operational, technical, and clinical factors is critical for patient quality and safety with this modality.

Inhibition of Jun N-terminal kinase (JNK) enhances glucocorticoid receptor-mediated function in mouse hippocampal HT22 cells.

Mitogen-activated protein kinases (MAPKs), including Jun N-terminal kinase (JNK), promote inflammatory and proliferative responses to infection and other environmental stimuli including stress. Relevant to negative regulation of inflammatory pathways by glucocorticoids and the development of glucocorticoid resistance (observed in inflammatory disorders as well as certain neuropsychiatric disorders such as major depression), activation of JNK has been reported to inhibit glucocorticoid receptor (GR) function. In this study, the role of JNK pathways in modulating GR function was further investigated. Treatment of mouse hippocampal (HT22) cells with the selective JNK inhibitor, SP-600125 (0.1-10 microM), resulted in dose-dependent induction of GR-mediated MMTV-luciferase activity. SP-600125 also significantly enhanced dexamethasone-induced MMTV-luciferase activity, while increasing GR binding to the glucocorticoid responsive element, both in the presence and absence of Dex. Similar effects were observed in mouse fibroblast cells (LMCAT), and in HT22 cells treated with a JNK specific antisense oligonucleotide. The induction of GR-mediated function by SP-600125 was not due to altered cytosolic GR binding or GR protein expression or enhancement of GR nuclear translocation as determined by Western blot. Taken together, the data indicate that constitutive expression of JNK plays a tonic inhibitory role in GR function, which is consistent with findings that activation of JNK pathways inhibits GR. The data also identify potential pathways involved in the pathogenesis of the glucocorticoid resistance found in certain chronic immune/inflammatory diseases and subgroups of patients with major depression. Moreover, JNK pathways may represent a therapeutic target for normalization of GR function in these disorders.