In this statewide analysis, we found that EMTs had a significantly higher Mortality Odds Ratio due to suicide compared to non-EMTs. Further research is necessary to identify the underlying causes of suicide among EMTs and to develop effective prevention strategies.
We propose a new healthcare data exchange platform for research centers, hospitals and healthcare institutions. Our model is based on a federated blockchain network that interconnect the healthcare institutions and orchestrate the data life cycle from the data publication to the data consumption. The blockchain is responsabible to keep the traceability of the whole process and we use a specially designed smart contract to control the data sharing process. Moreover, we provide the means to enforce GDPR and thus achieve a GDPR compliant model. CCS CONCEPTS• Computer systems organization → Distributed architectures; • General and reference → Design; • Software and its engineering → Peer-to-peer architectures; • Theory of computation → Cryptographic protocols.
Heart failure is a debilitating illness that is characterized by excessive extracellular matrix (ECM) accumulation. Cardiac fibroblasts maintain homeostasis of collagen production and degradation ‐ a tightly regulated process that is critical for normal heart function. Pathological cardiac fibrosis results from uncontrolled proliferation of fibroblasts and excessive production of ECM proteins including collagens – which may be mediated by reactive oxygen species. The pro‐fibrotic effects are mediated by a differentiated and activated fibroblast phenotype termed a myofibroblast. We have previously shown that angiotensin converting enzyme (ACE) inhibitors induce apoptosis of 30% of cardiac fibroblasts in adult spontaneously hypertensive rats (SHR). In addition, a 10% (p<0.05) reduction in left ventricular mass, compared to untreated control and was accompanied by a 12% (p<0.05) reduction in left ventricular DNA content. Moreover, transient ACE inhibition induces persistent changes that protect against future fibrosis and macrophage infiltration in response to injury. Based on these findings, we hypothesize that cardiac fibroblasts isolated from SHR previously treated with an ACE inhibitor will display a less fibrogenic phenotype than those isolated from control SHR. Adult male SHR were treated for 2 weeks with the ACE inhibitor enalapril (30mg/kg per day, p.o.) or water followed by a 2‐week washout period. Cardiac fibroblast were isolated from left ventricle and cultured to P1. Fibroblasts isolated from SHR previously treated with enalapril secreted significantly higher levels of TGF‐β1 in media (↑30%, p<0.05), and tended to have increased expression of the matricellular protein periostin (↑62%, p=0.052) relative to fibroblasts isolated from untreated SHR. Levels of the pro‐oxidant enzyme NOX2 were not different between treatment groups. Taken together, our data demonstrate that cardiac fibroblasts isolated from SHR that were transiently treated in vivo with an ACE inhibitor are different from those isolated from control SHR hearts. Future studies will further determine the extent to which ECM regulatory proteins differ in cells isolated from ACE inhibitor treated rats, and the response of these cells to an in vitro pro‐fibrotic stimulus. We predict that this altered cell population is primarily responsible for the cardio‐protection that we have shown to persist even after stopping ACE inhibitor treatment.Support or Funding InformationFunding: Springboard Grant, UA College of Medicine – PhoenixThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
In response to hypertensive stimuli, like angiotensin II (AngII), cardiac fibroblasts (CFs) transform into an activated phenotype, which triggers increased collagen deposition and pro‐inflammatory signals. Transforming growth factor beta 1 (TGF‐β1) and reactive oxygen species are important modulators of AngII‐induced cardiac fibrosis and CF activation. The extent to which the AngII‐induced changes in CF phenotype persist in the absence of ongoing stimulation is not known. The objective of the present study was to determine the persistent impact of chronic AngII infusion on CF phenotype. Specifically, we performed an in vitro characterization of CFs isolated from rats chronically treated with AngII (in vivo) or saline (vehicle) and investigated acute (in vitro) responses to AngII thereafter. Adult male SD rats were administered AngII (200 ng/kg/min) or saline for 4 weeks. In half of the rats in each group, we measured mean arterial pressure (MAP), weighed the left ventricle (LV), and fixed a section of LV for assessment of collagen deposition (Sirius Red). In remaining rats, CFs were isolated and passaged to P1. CFs were treated in vitro with AngII (1uM) or vehicle for 72 hr. TGF‐β1 and monocyte chemoattractant protein 1 (MCP‐1) were assessed in culture media. Expression of pro‐/anti‐oxidant proteins NADPH oxidase 2 (Nox2), catalase and superoxide dismutase 1 (SOD1) were determined by western blot. Ang II increased MAP (43%, p<0.05), LV/BW (30%, p<0.05), and LV collagen deposition. TGF‐β1 release was not different from CFs isolated from saline vs. AngII infused rats. However, in vitro incubation with AngII significantly increased TGF‐β1 secretion in all CFs. CFs isolated from AngII‐infused rats secreted elevated levels of MCP‐1 (p<0.05), when compared to control CFs. MCP‐1 levels were not further modified by acute AngII treatment. Basal expression of Nox2, SOD1, and catalase was similar between CFs isolated from control vs. AngII‐infused rats. Acute AngII tended to increase Nox2 expression in CFs isolated from vehicle and AngII‐treated rats, whereas AngII only increased SOD1 expression (46%, p<0.05) in CFs from AngII‐infused rats. In vitro stimulation with AngII tended to increase catalase in CFs isolated from control rats, but reduced (20%, p<0.05) expression in CFs isolated from AngII infused rats. Taken together, these data demonstrate that CFs isolated from an actively remodeling myocardium continue to secrete elevated levels of MCP‐1, but not TGF‐β1, in vitro. Moreover, CFs from AngII‐infused rats displayed altered expression of antioxidant enzymes following AngII in vitro, which may play a role in worsened inflammatory signaling and resultant pro‐fibrotic activity. Future studies will further elucidate the fibrotic and inflammatory characteristics of CFs from the remodeling myocardium and determine the extent to which this persistent phenotype alters the future responsiveness to a pathogenic stimulus.Support or Funding InformationSpringboard Grant, UA College of Medicine – PhoenixThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Background: The advent of highly sensitive End-Tidal CO2 (ETCO2) sensors allows effective monitoring of intubated patients in many emergency care settings, including EMS. Previous work has explored the use of ETCO2 monitoring in non-intubated patients with sensors placed in the nares. However, nothing is known about the effect of passive oxygen delivery [nasal cannula (NC) or non-rebreather mask (NRB)] on ETCO2 measurement. Objective: To compare ETCO2 measurements in non-intubated Traumatic Brain Injury (TBI) patients receiving O2 via NC vs NRB in the prehospital setting. Methods: A subset of major TBI cases (CDC Barell Matrix Type-1) in the Excellence in Prehospital Injury Care (EPIC) TBI Study (NIH/NINDS-1R01NS071049; ClinicalTrials.gov-NCT01339702) were evaluated 4/13-3/17). Non-intubated cases from 6 EMS agencies providing monitor data (Philips MRx) were included when continuous ETCO2 data were available. Statistics: Two-tailed t test, α = 0.05. Results: The 104 included cases had median age of 50.5 (range: 9-91; male: 67%). 39 (37.5%) received O2 via NC and 65 (62.5%) via NRB. Mean ETCO2: NC cases: 27.7 mmHg (95% CI: 25.7, 29.8); NRB: 30.0 (28.1, 31.8; p=0.132). There were also no significant differences among the mean lowest recorded values (p=0.449) or the mean highest values (p=0.275). Conclusion: We believe this is the first report comparing ETCO2 values based upon the method of passive O2 delivery in non-intubated patients. The minor differences between NC vs NRB-oxygenated patients was neither statistically nor clinically significant. This is surprising since: 1) the O2 flow rates and 2) the open-air (NC) vs mask (NRB) delivery methods are so dramatically different. Future study is needed to identify the clinical implications of using noninvasive ETCO2 measurement as a tool for monitoring ventilatory status and changes in non-intubated TBI (and other) patients.
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