Financial impact of reducing door-to-balloon time in ST-elevation myocardial infarction: a single hospital experience

<p>Abstract</p> <p>Background</p> <p>The impact of reducing door-to-balloon time on hospital revenues, costs, and net income is unknown.</p> <p>Methods</p> <p>We prospectively determined the impact on hospital finances of (1) emergency department physician activation of the catheterization lab and (2) immediate transfer of the patient to an immediately available catheterization lab by an in-house transfer team consisting of an emergency department nurse, a critical care unit nurse, and a chest pain unit nurse. We collected financial data for 52 consecutive ST-elevation myocardial infarction patients undergoing emergency percutaneous intervention from October 1, 2004–August 31, 2005 and compared this group to 80 consecutive ST-elevation myocardial infarction patients from September 1, 2005–June 26, 2006 after protocol implementation.</p> <p>Results</p> <p>Per hospital admission, insurance payments (hospital revenue) decreased ($35,043 ±$36,670 vs. $25,329 ±$16,185, P = 0.039) along with total hospital costs ($28,082 ±$31,453 vs. $18,195 ±$9,242, P = 0.009). Hospital net income per admission was unchanged ($6962 vs.$7134, P = 0.95) as the drop in hospital revenue equaled the drop in costs. For every $1000 reduction in total hospital costs, insurance payments (hospital revenue) dropped$1077 for private payers and $1199 for Medicare/Medicaid. A decrease in hospital charges ($70,430 ± $74,033 vs.$53,514 ± $23,378, P = 0.059), diagnosis related group relative weight (3.7479 ± 2.6731 vs. 2.9729 ± 0.8545, P = 0.017) and outlier payments with hospital revenue>$100,000 (7.7% vs. 0%, P = 0.022) all contributed to decreasing ST-elevation myocardial infarction hospitalization revenue. One-year post-discharge financial follow-up revealed similar results: Insurance payments: $49,959 ±$53,741 vs. $35,937 ±$23,125, P = 0.044; Total hospital costs: $39,974 ±$37,434 vs. $26,778 ±$15,561, P = 0.007; Net Income: $9984 vs.$9159, P = 0.855.</p> <p>Conclusion</p> <p>All of the financial benefits of reducing door-to-balloon time in ST-elevation myocardial infarction go to payers both during initial hospitalization and after one-year follow-up.</p> <p>Trial Registration</p> <p><b>ClinicalTrials.gov ID</b>: NCT00800163</p

A comparison of SERS and MEF of rhodamine 6G on a gold substrate

Rhodamine 6G is spin-cast onto gold surfaces and the reflectance, emission, excitation, and SERS spectra are reported. Electron microscopy shows that the particle sizes of the gold are uniform for all preparations. Reflection spectra demonstrate the spectroscopic signature for Rh6G aggregates for thicker films and that the gold plasmon band shifts due to the refractive index change on the surface. The intensity of the SERS spectra increases with increasing surface coverage but the change is nonlinear between submonolayer and multilayer surface densities. The SERS resonance frequencies are unchanged as a function of Rh6G thickness, indicating that there is no coupling between Rh6G molecules in the ground state. The emission spectra behave unexpectedly as a function of Rh6G coverage. At submonolayer coverage the emission is relatively strong, decreases as the surface density increases to a monolayer, and then increases as the Rh6G thickness increases. Excitation spectra demonstrate that the emitting species at low surface density is monomeric but for thicker layers the moiety responsible for emission is Rh6G excited state aggregates. For the thicker films, the Rh6G acts as its own dielectric layer for metal enhanced fluorescence of the aggregates, which is the first example of a system where the fluorophore acts as its own dielectric for metal enhanced fluorescence. The intensity of the aggregate emission on gold intensity is three times of that found when Rh6G is deposited on glass. The gold induces emission in the Rh6G excited state aggregates that are quenched in the absence of the plasmon field

Accurate Prediction of Secreted Substrates and Identification of a Conserved Putative Secretion Signal for Type III Secretion Systems

The type III secretion system is an essential component for virulence in many Gram-negative bacteria. Though components of the secretion system apparatus are conserved, its substrates—effector proteins—are not. We have used a novel computational approach to confidently identify new secreted effectors by integrating protein sequence-based features, including evolutionary measures such as the pattern of homologs in a range of other organisms, G+C content, amino acid composition, and the N-terminal 30 residues of the protein sequence. The method was trained on known effectors from the plant pathogen Pseudomonas syringae and validated on a set of effectors from the animal pathogen Salmonella enterica serovar Typhimurium (S. Typhimurium) after eliminating effectors with detectable sequence similarity. We show that this approach can predict known secreted effectors with high specificity and sensitivity. Furthermore, by considering a large set of effectors from multiple organisms, we computationally identify a common putative secretion signal in the N-terminal 20 residues of secreted effectors. This signal can be used to discriminate 46 out of 68 total known effectors from both organisms, suggesting that it is a real, shared signal applicable to many type III secreted effectors. We use the method to make novel predictions of secreted effectors in S. Typhimurium, some of which have been experimentally validated. We also apply the method to predict secreted effectors in the genetically intractable human pathogen Chlamydia trachomatis, identifying the majority of known secreted proteins in addition to providing a number of novel predictions. This approach provides a new way to identify secreted effectors in a broad range of pathogenic bacteria for further experimental characterization and provides insight into the nature of the type III secretion signal