ABSTRACT
The COVID-19 national emergency has led to surging care demand and the need for unprecedented telehealth expansion. Rapid telehealth expansion can be especially complex for pediatric patients. From the experience of a large academic medical center, this report describes a pathway for efficiently increasing capacity of remote pediatric enrollment for telehealth while fulfilling privacy, security, and convenience concerns. The design and implementation of the process took 2 days. Five process requirements were identified: efficient enrollment, remote ability to establish parentage, minimal additional work for application processing, compliance with guidelines for adolescent autonomy, and compliance with institutional privacy and security policies. Weekly enrollment subsequently increased 10-fold for children (age 0-12 years) and 1.2-fold for adolescents (age 13-17 years). Weekly telehealth visits increased 200-fold for children and 90-fold for adolescents. The obstacles and solutions presented in this report can provide guidance to health systems for similar challenges during the COVID-19 response and future disasters.
Subject(s)
Betacoronavirus , Coronavirus Infections/therapy , Patient Portals , Pneumonia, Viral/therapy , Telemedicine/statistics & numerical data , Adolescent , COVID-19 , Child , Child, Preschool , Confidentiality , Consumer Health Informatics , Female , Humans , Infant , Male , Pandemics , Parents , SARS-CoV-2 , Telemedicine/trends , TennesseeABSTRACT
Glioblastoma (GBM) and lower grade gliomas (LGG) are the most common primary malignant brain tumors and are resistant to current therapies. Genomic analyses reveal that signature genetic lesions in GBM and LGG include copy gain and amplification of chromosome 7, amplification, mutation, and overexpression of receptor tyrosine kinases (RTK) such as EGFR, and activating mutations in components of the PI3K pathway. In Drosophila melanogaster, constitutive co-activation of RTK and PI3K signaling in glial progenitor cells recapitulates key features of human gliomas. Here we use this Drosophila glioma model to identify death-associated protein kinase (Drak), a cytoplasmic serine/threonine kinase orthologous to the human kinase STK17A, as a downstream effector of EGFR and PI3K signaling pathways. Drak was necessary for glial neoplasia, but not for normal glial proliferation and development, and Drak cooperated with EGFR to promote glial cell transformation. Drak phosphorylated Sqh, the Drosophila ortholog of nonmuscle myosin regulatory light chain (MRLC), which was necessary for transformation. Moreover, Anillin, which is a binding partner of phosphorylated Sqh, was upregulated in a Drak-dependent manner in mitotic cells and colocalized with phosphorylated Sqh in neoplastic cells undergoing mitosis and cytokinesis, consistent with their known roles in nonmuscle myosin-dependent cytokinesis. These functional relationships were conserved in human GBM. Our results indicate that Drak/STK17A, its substrate Sqh/MRLC, and the effector Anillin/ANLN regulate mitosis and cytokinesis in gliomas. This pathway may provide a new therapeutic target for gliomas.Significance: These findings reveal new insights into differential regulation of cell proliferation in malignant brain tumors, which will have a broader impact on research regarding mechanisms of oncogene cooperation and dependencies in cancer.See related commentary by Lathia, p. 1036.
