Navigating Transitions in Oncology Care: From Emergency Department to Outpatient Clinic.

OBJECTIVE: This quality improvement project was a collaborative effort with Penn Medicine's emergency department (ED) and oncology nurse navigators (ONNs). The goal of the project was to streamline patient transitions from the ED to the outpatient oncology clinic by developing a standardized referral process. The main objectives were to simplify and automate the referral process using the electronic medical record, improve multidisciplinary communication across the care continuum, ensure timely follow-up, and address barriers to oncology care. METHODS: The ED providers placed a consult to ONNs. The ONNs reached out to the patient within 48 hours of the consult. They maintained a database of patient referrals and collected information such as patient demographics, reason for referral, insurance, and patient outcomes. RESULTS: The ED providers referred 204 patients to the ONNs from April 2022 to September 2023. The development of a standardized referral process from the ED to the outpatient oncology clinic proved successful. Of the patients referred, the ONNs facilitated 98 cancer diagnoses and 80 of those patients are receiving oncology care at Penn Medicine. The median time to the patient's first appointments was seven days, diagnosis was 15 days, and treatment initiation occurred within 32 days. CONCLUSION: The project team achieved their goal of facilitating timely access to oncology care, ensuring continuity, and addressing patient-specific barriers. IMPLICATIONS FOR NURSING PRACTICE: This quality improvement initiative highlights the ONNs' role in enhancing access and equity in cancer care delivery. The success of the project underscores the ONN's expertise and leadership in addressing healthcare disparities in oncology care. Collaboratively, the teams created a new referral workflow improving care transitions from the ED to the outpatient oncology clinic. The project sets a precedent for optimizing patient care transitions, demonstrating the positive impact of ONNs as key members of the multidisciplinary healthcare team.

Lupus-like autoantibody development in rabbits and mice after immunization with EBNA-1 fragments.

Epstein-Barr virus has been implicated in the etiology of systemic lupus erythematosus (SLE) through serologic and immunologic studies. A potential mechanism for this influence is through molecular mimicry. The EBV nuclear antigen EBNA-1 contains a region, PPPGRRP, with considerable homology to the initial sequence targeted by antibodies in Sm B' autoimmunity, PPPGMRPP. This study examined whether immunization of rabbits and mice with peptides containing the PPPGRRP sequence from EBNA-1 constructed on a poly-lysine backbone was able to drive the development of autoantibodies against the Smith antigen (Sm) and the related antigenic complex, the U1 nuclear ribonucleoproteins (nRNPs). PPPGRRP immunization, and immunization with an EBNA-1 fragment containing PPPGRRP, led to autoantibodies in both rabbits and mice at high frequency (83% of rabbits and 43% of mice). Five out of six immunized rabbits developed either leucopenia or lymphopenia or both. The fine specificity of antibody binding against the lupus-associated autoantigens Sm B', nRNP A, and nRNP C after immunization with the EBNA-1-derived peptides was very similar to the early antibody binding patterns against these proteins in human SLE. This similarity, as well as the prevalence of autoimmunity after immunization with these peptides, identifies PPPGRRP as a strong candidate for molecular mimicry in SLE etiology.

Anti-nuclear antibody production and autoimmunity in transgenic mice that overexpress the transcription factor Bright.

The B cell-restricted transcription factor, B cell regulator of Ig(H) transcription (Bright), up-regulates Ig H chain transcription 3- to 7-fold in activated B cells in vitro. Bright function is dependent upon both active Bruton's tyrosine kinase and its substrate, the transcription factor, TFII-I. In mouse and human B lymphocytes, Bright transcription is down-regulated in mature B cells, and its expression is tightly regulated during B cell differentiation. To determine how Bright expression affects B cell development, transgenic mice were generated that express Bright constitutively in all B lineage cells. These mice exhibited increases in total B220(+) B lymphocyte lineage cells in the bone marrow, but the relative percentages of the individual subpopulations were not altered. Splenic immature transitional B cells were significantly expanded both in total cell numbers and as increased percentages of cells relative to other B cell subpopulations. Serum Ig levels, particularly IgG isotypes, were increased slightly in the Bright-transgenic mice compared with littermate controls. However, immunization studies suggest that responses to all foreign Ags were not increased globally. Moreover, 4-wk-old Bright-transgenic mice produced anti-nuclear Abs. Older animals developed Ab deposits in the kidney glomeruli, but did not succumb to further autoimmune sequelae. These data indicate that enhanced Bright expression results in failure to maintain B cell tolerance and suggest a previously unappreciated role for Bright regulation in immature B cells. Bright is the first B cell-restricted transcription factor demonstrated to induce autoimmunity. Therefore, the Bright transgenics provide a novel model system for future analyses of B cell autoreactivity.