Physical therapy in the Emergency Department: A prospective cohort study from an Alternatives to Opioids program.

Objective: Musculoskeletal pain complaints are common in the emergency department (ED). The objective of this study was to determine the impact of physical therapy (PT) in the ED on pain and ED return. Methods: A prospective cohort study was performed with those presenting to the ED or Urgent Care at a single academic center for musculoskeletal pain between November 2020 and December 2022. All patients were referred to outpatient PT. During business hours, PT was available to begin treatment in the ED. Long-term follow-up was performed using the electronic health records. Statistical analyses included descriptive and non-parametric pairwise comparisons, Fisher's exact test, and multiple logistic regression. Results: A total of 974 patients were included in the study with 553 completing optional surveys. Back pain was most common. Pain was reduced at ED discharge for all patients, but pain was significantly improved if patients saw PT in the ED. Patients in the ED were less likely to keep their outpatient PT appointments than others, but importantly, patients who saw PT in the ED were less likely to return to the ED for the same complaint up to 1 year later. Those who kept PT appointments were likely to establish or maintain healthcare outside emergency services later. Conclusions: Initiating PT in this ED reduces pain at ED discharge. However, patients who utilized PT were more likely to later utilize health care resources outside of emergency services. Those who saw PT in this ED were less likely to return to the ED for the same complaint up to 1 year later.

Isolation of circulating endothelial cells provides tool to determine endothelial cell senescence in blood samples.

Circulating endothelial cells (CEC) are arising as biomarkers for vascular diseases. However, whether they can be utilized as markers of endothelial cell (EC) senescence in vivo remains unknown. Here, we present a protocol to isolate circulating endothelial cells for a characterization of their senescent signature. Further, we characterize different models of EC senescence induction in vitro and show similar patterns of senescence being upregulated in CECs of aged patients as compared to young volunteers. Replication-(ageing), etoposide-(DNA damage) and angiotensin II-(ROS) induced senescence models showed the expected cell morphology and proliferation-reduction effects. Expression of senescence-associated secretory phenotype markers was specifically upregulated in replication-induced EC senescence. All models showed reduced telomere lengths and induction of the INK4a/ARF locus. Additional p14ARF-p21 pathway activation was observed in replication- and etoposide-induced EC senescence. Next, we established a combined magnetic activated- and fluorescence activated cell sorting (MACS-FACS) based protocol for CEC isolation. Interestingly, CECs isolated from aged volunteers showed similar senescence marker patterns as replication- and etoposide-induced senescence models. Here, we provide first proof of senescence in human blood derived circulating endothelial cells. These results hint towards an exciting future of using CECs as mirror cells for in vivo endothelial cell senescence, of particular interest in the context of endothelial dysfunction and cardiovascular diseases.