ObjectiveDisparities in treatment outcomes for traumatic injury are an important concern for care providers and policy makers. Factors that may influence these disparities include differences in risk exposure based on neighbourhood of residence and differences in quality of care between hospitals in different areas. This study examines geographical disparities within a single region: the Detroit metropolitan area.DesignData on all trauma admissions between 2006 and 2014 were obtained from the Michigan State Inpatient Database. Admissions were grouped by patient neighbourhood of residence and admitting hospital. Generalised linear mixed modelling procedures were used to determine the extent of shared variance based on these two levels of categorisation on three outcomes. Patients with trauma due to common mechanisms (falls, firearms and motor vehicle traffic) were examined as additional subgroups.Setting66 hospitals admitting patients for traumatic injury in the Detroit metropolitan area during the period from 2006 to 2014.Participants404 675 adult patients admitted for treatment of traumatic injury.Outcome measuresIn-hospital mortality, length of stay and hospital charges.ResultsIntraclass correlation coefficients indicated that there was substantial shared variance in outcomes based on hospital, but not based on neighbourhood of residence. Among all injury types, hospital-level differences accounted for 12.5% of variance in mortality risk, 28.5% of variance in length of stay and 32.2% of variance in hospital charges. Adjusting the results for patient age, injury severity, mechanism and comorbidities did not result in significant reduction in the estimated variance at the hospital level.ConclusionsBased on these data, geographical disparities in trauma treatment outcomes were more strongly attributable to differences in access to quality hospital care than to risk factors in the neighbourhood environment. Transfer of high-risk cases to hospitals with greater institutional experience in the relevant area may help address mortality disparities in particular.
e23012 Background: Pulmonary metastases still remains the leading cause of mortality in osteosarcoma, with a 5-year survival rate of less than 30%. 17-β estradiol and testosterone are known to promote tumorigenesis and metastasis in other cancers, but its role in osteosarcoma tumorigenesis and metastasis is unclear. An understanding of the mechanism that these hormones have in osteosarcoma tumorigenesis and metastasis will lead to new therapeutic strategies using currently available targeted therapies used in breast and prostate cancer. Methods: We began by assessing the in vitro characteristics of two human osteosarcoma cell lines treated with 17-β estradiol or testosterone via proliferation and invasion assays. For the in vivo experiments, NCR nu/nu mice were injected with two luciferase-tagged human osteosarcoma cell lines and treated with 17-β estradiol and testosterone slow-release pellets. We first injected the mice subcutaneously and monitored tumor growth via caliper measurements. In the second experiment we injected the cell lines intratibially and monitored primary tumor growth in the bone and monitored metastasis formation in the lungs via IVIS bioluminescent imaging. Quantification of luciferase signal (photons/second) in the lungs was performed via the Xenogen Living Image software. H&E and immunohistochemistry for luciferase expression was performed on lung tissue to quantify tumor burden in the lungs. Statistical analysis was performed using Graphpad Prism. Results: Treatment with 17-β estradiol and testosterone increased cell proliferation and invasion in a dose-dependent manner. We observed increased tumor growth with both 17-β estradiol and testosterone in the subcutaneous model. In the intratibial experiment, testosterone increases primary tumor growth, but has no effect on metastasis. 17-β estradiol decreases primary tumor growth, but increases metastasis in a cell line independent manner. Conclusions: This study demonstrates a novel role for the puberty-related sex steroid hormones, 17-β estradiol and testosterone, in osteosarcoma tumor growth and metastasis. Uncovering the mechanism behind this phenomenon will uncover new therapeutic options for this devastating disease.
No abstract
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.