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Other TitlesCenter to Advance Chronic Pain Research and Chronic Pain: Quick Facts
KeywordUniversity of Maryland, Baltimore. Center to Advance Chronic Pain
Center to Advance Chronic Pain Research
Identifier to cite or link to this itemhttp://hdl.handle.net/10713/11191
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An in vitro model yields ‘importin’ new insights into chronic traumatic encephalopathy: damaged astrocytes stop ‘thrombospondin’ to the injury An Editorial Highlight for ‘Defective synthesis and release of astrocytic thrombospondin‐1 mediates the neuronal TDP‐43 proteinopathy, resulting in defects in neuronal integrity associated with chronic traumatic encephalopathy: in vitro studies’Jaber, S.M.; Polster, B.M. (Blackwell Publishing Ltd, 2017)This Editorial highlights a study by Jayakumar and colleagues (2016) in the current issue of Journal of Neurochemistry. The authors introduce an in vitro model of chronic traumatic encephalopathy (CTE) to explore the mechanistic underpinnings of CTE pathogenesis, including investigation of how traumatized astrocytes affect traumatized neurons through the release of secreted factors. The model recapitulates two key features of the human post-mortem CTE brain: neuronal tauopathy and TDP-43 proteinopathy—the respective accretion of hyperphosphorylated tau and cytoplasmic hyperphosphorylated and ubiquitinated TDP-43. Oxidative stress and casein kinase 1 episilon (CK1ε) are identified as key upstream regulators of cytoplasmic TDP-43 phosphorylation, and this phosphorylation is found to correlate with decreased importin-β protein level and a decline in synaptic integrity. RNA silencing of importin-β is sufficient to mimic both the phospho-TDP-43 accumulation and synaptic injury observed after mild in vitro trauma. Strikingly, Jayakumar et al. find that thrombospondin-1 (TSP-1), a protein secreted by traumatized astrocytes at elevated levels during the initial 5 days after damage, can attenuate CK1ε phosphorylation of TDP-43 and synaptic injury. However, TSP-1 secretion by astrocytes is lost at 10–15 days post-injury, and neurons succumb to unchecked TDP-43 pathogenesis.
Cardiac Biomarkers and Risk of Incident Heart Failure in Chronic Kidney Disease: The CRIC (Chronic Renal Insufficiency Cohort) StudyChristenson, R.; Seliger, S.; CRIC, Study, Investigators (American Heart Association, 2019)Background Cardiac biomarkers may signal mechanistic pathways involved in heart failure (HF), a leading complication in chronic kidney disease. We tested the associations of NT-proBNP (N-terminal pro-B-type natriuretic peptide), high-sensitivity troponin T (hsTnT), galectin-3, growth differentiation factor-15 (GDF-15), and soluble ST2 (sST2) with incident HF in chronic kidney disease. Methods and Results We examined adults with chronic kidney disease enrolled in a prospective, multicenter study. All biomarkers were measured at baseline. The primary outcome was incident HF. Secondary outcomes included HF with preserved ejection fraction (EF?50%) and reduced ejection fraction (EF<50%). Cox models were used to test the association of each cardiac biomarker with HF, adjusting for demographics, kidney function, cardiovascular risk factors, and medication use. Among 3314 participants, all biomarkers, with the exception of galectin-3, were significantly associated with increased risk of incident HF (hazard ratio per SD higher concentration of log-transformed biomarker): NT-proBNP (hazard ratio, 2.07; 95% CI, 1.79-2.39); hsTnT (hazard ratio, 1.38; 95% CI, 1.21-1.56); GDF-15 (hazard ratio, 1.44; 95% CI, 1.26-1.66) and sST2 (hazard ratio, 1.19; 95% CI, 1.05-1.35). Higher NT-proBNP, hsTnT, and GDF-15 were also associated with a greater risk of HF with reduced EF; while higher NT-proBNP GDF-15 and sST2 were associated with HF with preserved EF. Galectin-3 was not associated with either HF with reduced EF or HF with preserved EF. Conclusions In chronic kidney disease, elevations of NT-proBNP, hsTnT, GDF-15, sST2 were associated with incident HF. There was a borderline association of galectin-3 with incident HF. NT-proBNP and hsTnT were more strongly associated with HF with reduced EF, while the associations of the newer biomarkers GDF-15 and sST2 were stronger for HF with preserved EF.
Enhancing Nursing Skills to Care for Patients with Chronic Obstructive Pulmonary DiseaseWatties-Daniels, A. Denyce (2017)Best practices in the care of patients experiencing a deteriorating condition include identifying changes in patient condition and initiating prompt and effective interventions. Nurses frequently fail to recognize deteriorating conditions and serious exacerbation of symptoms and thus are limited in providing appropriate supportive care to patients with COPD. Innovative strategies, such as the implementation of clinical simulations, are reported to be effective in reinforcing essential clinical decision-making skills to assist nurses in developing the knowledge and skills to better recognize and intervene in the care of deteriorating conditions in patients with COPD. The purpose of this Doctor of Nursing Practice quality improvement project was to develop, implement and evaluate the use of two simulation experiences to assist registered nurses to recognize and intervene in deteriorating conditions in chronically ill adult patients with COPD. Simulation scenarios included the patient with exacerbation of COPD and the patient with a spontaneous pneumothorax as a result of COPD complications. A convenience sample of seven licensed registered nurses from diverse clinical backgrounds participating in a nursing orientation program at an urban, general adult medicine and surgical hospital in Baltimore, Maryland engaged in the project. The NLN/ Jeffries Simulation Theory and the INASCL Standards of Best Practices in Simulation provided the framework for the project. Utilizing the three phases of the simulation experience, the seven registered nurses were immersed in the two simulated clinical situations. Baseline knowledge of the care of the patient with COPD and spontaneous pneumothorax was assessed by administering a 10 item, paper-pencil pre-test aligned to the simulation objectives. The simulation experiences were evaluated using the Creighton Competency Evaluation Instrument (C-CEI) and a 10 item posttest. The clinical nurse educator and the DNP project director used the C-CEI tool to separately evaluate participant performance in each simulation experience. The project director with clinical nurse educator validation, set the competency score for the C-CEI at 75%. The scores on the C-CEI were collected as an aggregate of the nurses delivering care to the simulated patient. All groups of nurses scored above 75%. A T-test (n=7, p =.000) for dependent groups was used to evaluate whether students’ performance on the COPD and pneumothorax pre-test improved on the post-test. There was a statistically significant increase in the COPD and pneumothorax mean scores from the pre-test to the post-test. The completed DNP project supports the use of clinical simulation to train and remediate practicing nurses. The participating nurses were able to immerse themselves in a realistic clinical situation and care for the simulated patients in a safe environment as though the patients were real. The participating nurses could identify significant changes in patient condition and were competent in intervening and caring for the deteriorating conditions of a COPD patient. Evidence from this DNP quality improvement project supports the need for continued clinical work and program evaluation on the development, and implementation of hospital based clinical simulation programs for nurses.