BioMed Central Open Access Articles (UMKC)
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This collection contains open access articles from January 2003 to January 2015 written by UMKC faculty doing research in the sciences and deposited here via BioMed Central.
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Item National trends in hospital length of stay for acute myocardial infarction in China(2015-01-20) Li, Qian; Lin, Zhenqiu; Masoudi, Frederick A; Li, Jing; Li, Xi; Hernández-Díaz, Sonia; Nuti, Sudhakar V; Li, Lingling; Wang, Qing; Spertus, John A; Hu, Frank B; Krumholz, Harlan M.; Jiang, LixinAbstract Background China is experiencing increasing burden of acute myocardial infarction (AMI) in the face of limited medical resources. Hospital length of stay (LOS) is an important indicator of resource utilization. Methods We used data from the Retrospective AMI Study within the China Patient-centered Evaluative Assessment of Cardiac Events, a nationally representative sample of patients hospitalized for AMI during 2001, 2006, and 2011. Hospital-level variation in risk-standardized LOS (RS-LOS) for AMI, accounting for differences in case mix and year, was examined with two-level generalized linear mixed models. A generalized estimating equation model was used to evaluate hospital characteristics associated with LOS. Absolute differences in RS-LOS and 95% confidence intervals were reported. Results The weighted median and mean LOS were 13 and 14.6 days, respectively, in 2001 (n = 1,901), 11 and 12.6 days in 2006 (n = 3,553), and 11 and 11.9 days in 2011 (n = 7,252). There was substantial hospital level variation in RS-LOS across the 160 hospitals, ranging from 9.2 to 18.1 days. Hospitals in the Central regions had on average 1.6 days (p = 0.02) shorter RS-LOS than those in the Eastern regions. All other hospital characteristics relating to capacity for AMI treatment were not associated with LOS. Conclusions Despite a marked decline over the past decade, the mean LOS for AMI in China in 2011 remained long compared with international standards. Inter-hospital variation is substantial even after adjusting for case mix. Further improvement of AMI care in Chinese hospitals is critical to further shorten LOS and reduce unnecessary hospital variation.Item Neoadjuvant treatment of Dermatofibrosarcoma Protuberans of pancreas with Imatinib: case report and systematic review of literature(2014-08-06) Dhir, Mashaal; Crockett, David G; Stevens, Todd M; Silberstein, Peter T; Hunter, William J; Foster, Jason MAbstract Dermatofibrosarcoma Protuberans (DFSP) is a rare skin tumor, characterized by frequent local recurrence but is seldom metastatic. It is histologically characterized by storiform arrangement of spindle cells. Cytogenetically, most tumors are characterized by translocation 17:22 leading to overexpression of tyrosine kinase PDGFB which can be targeted with tyrosine kinase inhibitor, Imatinib. We describe the first case of unresectable pancreatic metastases from DFSP treated with neoadjuvant Imatinib and subsequently R0 metastectomy. Additionally, a comprehensive systematic review of DFSP pancreatic metastases and the current published data on the use of Imatinib in DFSP is summarized.Item Butyrylcholinesterase genotype and enzyme activity in relation to Gulf War illness: preliminary evidence of gene-exposure interaction from a case¿control study of 1991 Gulf War veterans(2015-01-09) Steele, Lea; Lockridge, Oksana; Gerkovich, Mary M; Cook, Mary R; Sastre, AntonioAbstract Background Epidemiologic studies have implicated wartime exposures to acetylcholinesterase (AChE)-inhibiting chemicals as etiologic factors in Gulf War illness (GWI), the multisymptom condition linked to military service in the 1991 Gulf War. It is unclear, however, why some veterans developed GWI while others with similar exposures did not. Genetic variants of the enzyme butyrylcholinesterase (BChE) differ in their capacity for metabolizing AChE-inhibiting chemicals, and may confer differences in biological responses to these compounds. The current study assessed BChE enzyme activity and BChE genotype in 1991 Gulf War veterans to evaluate possible association of this enzyme with GWI. Methods This case–control study evaluated a population-based sample of 304 Gulf War veterans (144 GWI cases, meeting Kansas GWI criteria, and 160 controls). BChE enzyme activity levels and genotype were compared, overall, in GWI cases and controls. Potential differences in risk associated with cholinergic-related exposures in theater were explored using stratified analyses to compare associations between GWI and exposures in BChE genetic and enzyme activity subgroups. Results Overall, GWI cases and controls did not differ by mean BChE enzyme activity level or by BChE genotype. However, for the subgroup of Gulf War veterans with less common, generally less active, BChE genotypes (K/K, U/AK, U/A, A/F, AK/F), the association of wartime use of pyridostigmine bromide (PB) with GWI (OR = 40.00, p = 0.0005) was significantly greater than for veterans with the more common U/U and U/K genotypes (OR = 2.68, p = 0.0001). Conclusions Study results provide preliminary evidence that military personnel with certain BChE genotypes who used PB during the 1991 Gulf War may have been at particularly high risk for developing GWI. Genetic differences in response to wartime exposures are potentially important factors in GWI etiology and should be further evaluated in conjunction with exposure effects.Item Separating signal from noise: the challenge of identifying useful biomarkers in sepsis(2014-03-17) McCulloh, Russell J; Spertus, John AAbstract Sepsis diagnosis remains based largely on clinical presentation despite significant advances in the understanding of underlying pathophysiology and host-pathogen interactions. The systematic review article by Zonneveld and colleagues in the previous issue of Critical Care describes another potential avenue of study for using biomarkers for sepsis diagnosis and prognostication. Soluble leukocyte adhesion molecules and their associated sheddase enzymes vary in detectable levels and activity in patients in relation to immunologic status, age, and systemic inflammation, including in the setting of sepsis. Unfortunately, studies of these molecules as diagnostic or prognostic aids (or both) in sepsis have thus far been disappointing. Zonneveld and colleagues propose two potential avenues to enhance the performance characteristics of soluble adhesion molecules and their sheddases in sepsis diagnosis and prognosis: (a) identifying age-adjusted normal values for soluble leukocyte adhesion molecules and their sheddases and (b) investigating simultaneous measurement of both soluble adhesion molecules and sheddases in integrated sepsis evaluation schema. This commentary discusses the proposed solutions of Zonneveld and colleagues in more detail and outlines additional considerations that should be addressed in order to develop robust and valid diagnostic and prognostic tools for clinicians managing patients with sepsis.Item Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB(2014-12-17) Touchberry, Chad D.; Silswal, Neerupma; Tchikrizov, Vladimir; Elmore, Christopher J.; Srinivas, Shubra; Akthar, Adil S.; Swan, Hannah K.; Wetmore, Lori A.; Wacker, Michael J.Abstract Background We have previously shown that the thromboxane (TXA2) receptor agonist, U46619, can directly induce ventricular arrhythmias that were associated with increases in intracellular calcium in cardiomyocytes. Since TXA2 is an inflammatory mediator and induces direct calcium changes in cardiomyocytes, we hypothesized that TXA2 released during ischemia or inflammation could also cause cardiac remodeling. Methods U46619 (0.1-10 μM) was applied to isolated adult mouse ventricular primary cardiomyocytes, mouse ventricular cardiac muscle strips, and cultured HL-1 cardiomyocytes and markers of hypertrophy and cell death were measured. Results We found that TXA2 receptors were expressed in ventricular cardiomyocytes and were functional via calcium imaging. U46619 treatment for 24 h did not increase expression of pathological hypertrophy genes (atrial natriuretic peptide, β-myosin heavy chain, skeletal muscle α-actin) and it did not increase protein synthesis. There was also no increase in cardiomyocyte size after 48 h treatment with U46619 as measured by flow cytometry. However, U46619 (0.1-10 μM) caused a concentration-dependent increase in cardiomyocyte death (trypan blue, MTT assays, visual cell counts and TUNEL stain) after 24 h. Treatment of cells with the TXA2 receptor antagonist SQ29548 and inhibitors of the IP3 pathway, gentamicin and 2-APB, eliminated the increase in cell death induced by U46619. Conclusions Our data suggests that TXA2 does not induce cardiac hypertrophy, but does induce cell death that is mediated in part by IP3 signaling pathways. These findings may provide important therapeutic targets for inflammatory-induced cardiac apoptosis that can lead to heart failure.