Hispanic Farmers Experience Shorter EMS Response Times but Longer Emergency Department Length of Stay Following Occupational Injuries.

BACKGROUND: Agriculture has the highest rate of fatal injuries by sector. Hispanic workers also experience more fatal work injuries than every other minority group combined. Pre-hospital and initial trauma evaluation represent an important marker to understand the impact of a trauma system. We sought to investigate whether Hispanic agricultural workers in the United States (US) experience disparities following traumatic occupational injuries in terms of pre-hospital and emergency department care. METHODS: We retrospectively analyzed the National Trauma Data Bank from 2012-2016 to understand differences between Hispanic and non-Hispanic farmers in Emergency Medical Services (EMS) response and transport times (minutes), transport mode, transfer rates, presentation to University or Level I trauma hospitals, Injury Severity Scores (ISS), length of stay (LOS) in the emergency department (ED, minutes) or hospital (days), need for the operating room (OR), admittance to the Intensive Care Unit (ICU), and mortality. RESULTS: A total of 6,161 farmers were included in our analyses (median age 47 years, females 7.0%). Multivariable analyses indicate differences regarding EMS response, EMS transport, and LOS in the ED. Rates of admission to the ICU, surgical operations, days on a ventilator, discharge from the hospital with supportive care, and mortality did not differ between groups. CONCLUSIONS: Non-Hispanic patients have longer median EMS response and total transport times. Hispanic patients have longer median LOS in the ED. However, the lack of significant differences in management variables other than EMS times and ED LOS indicate an equitable delivery of trauma care once patients were transferred from the ED.

Cross-talk between SIM2s and NFκB regulates cyclooxygenase 2 expression in breast cancer.

BACKGROUND: Breast cancer is a leading cause of cancer-related death for women in the USA. Thus, there is an increasing need to investigate novel prognostic markers and therapeutic methods. Inflammation raises challenges in treating and preventing the spread of breast cancer. Specifically, the nuclear factor kappa b (NFκB) pathway contributes to cancer progression by stimulating proliferation and preventing apoptosis. One target gene of this pathway is PTGS2, which encodes for cyclooxygenase 2 (COX-2) and is upregulated in 40% of human breast carcinomas. COX-2 is an enzyme involved in the production of prostaglandins, which mediate inflammation. Here, we investigate the effect of Singleminded-2s (SIM2s), a transcriptional tumor suppressor that is implicated in inhibition of tumor growth and metastasis, in regulating NFκB signaling and COX-2. METHODS: For in vitro experiments, reporter luciferase assays were utilized in MCF7 cells to investigate promoter activity of NFκB and SIM2. Real-time PCR, immunoblotting, immunohistochemistry, and chromatin immunoprecipitation assays were performed in SUM159 and MCF7 cells. For in vivo experiments, MCF10DCIS.COM cells stably expressing SIM2s-FLAG or shPTGS2 were injected into SCID mice and subsequent tumors harvested for immunostaining and analysis. RESULTS: Our results reveal that SIM2 attenuates the activation of NFκB as measured using NFκB-luciferase reporter assay. Furthermore, immunostaining of lysates from breast cancer cells overexpressing SIM2s showed reduction in various NFκB signaling proteins, as well as pAkt, whereas knockdown of SIM2 revealed increases in NFκB signaling proteins and pAkt. Additionally, we show that NFκB signaling can act in a reciprocal manner to decrease expression of SIM2s. Likewise, suppressing NFκB translocation in DCIS.COM cells increased SIM2s expression. We also found that NFκB/p65 represses SIM2 in a dose-dependent manner, and when NFκB is suppressed, the effect on the SIM2 is negated. Additionally, our ChIP analysis confirms that NFκB/p65 binds directly to SIM2 promoter site and that the NFκB sites in the SIM2 promoter are required for NFκB-mediated suppression of SIM2s. Finally, overexpression of SIM2s decreases PTGS2 in vitro, and COX-2 staining in vivo while decreasing PTGS2 and/or COX-2 activity results in re-expression of SIM2. CONCLUSION: Our findings identify a novel role for SIM2s in NFκB signaling and COX-2 expression.