The Effect of Soft Budget Constraints on Access and Quality in Hospital Care

Given an increasingly complex web of financial pressures on providers, studies have examined how the hospitals' overall financial health affect different aspects of hospital operation. In our study, we analyze this issue focusing on hospital access and quality by introducing an important aspect of the financial incentives, soft budget constraints (SBC), that takes into account both hospital's current and past financial health as well as their expected financial outlook (i.e., whether there is a sponsoring organization to bail them out). We develop a conceptual framework of SBC by considering the resultant incentives on cost control and quality improvement innovations; and examine the effect of SBC on the following aspects of access and quality: safety net service survival and AMI mortality rates. We find that hospitals with softer budget constraints are less likely to shut down safety net services. In addition, hospitals with softer budget constraints appear to have better mortality outcomes, suggesting that the reduced incentive to engage in cost control innovation as the result of SBC outweighs the dampening effect of quality improvement innovation.

Simulated changes in salinity in the York and Chickahominy Rivers from projected sea-level rise in Chesapeake Bay

As a result of climate change and variability, sea level is rising throughout the world, but the rate along the east coast of the United States is higher than the global mean rate. The U.S. Geological Survey, in cooperation with the City of Newport News, Virginia, conducted a study to evaluate the effects of possible future sea-level rise on the salinity front in two tributaries to Chesapeake Bay, the York River, and the Chickahominy/James River estuaries. Numerical modeling was used to represent sea-level rise and the resulting hydrologic effects. Estuarine models for the two tributaries were developed and model simulations were made by use of the Three-Dimensional Hydrodynamic-Eutrophication Model (HEM-3D), developed by the Virginia Institute of Marine Science. HEM-3D was used to simulate tides, tidal currents, and salinity for Chesapeake Bay, the York River and the Chickahominy/James River. The three sea-level rise scenarios that were evaluated showed an increase of 30, 50, and 100 centimeters (cm). Model results for both estuaries indicated that high freshwater river flow was effective in pushing the salinity back toward Chesapeake Bay. Model results indicated that increases in mean salinity will greatly alter the existing water-quality gradients between brackish water and freshwater. This will be particularly important for the freshwater part of the Chickahominy River, where a drinking-water-supply intake for the City of Newport News is located. Significant changes in the salinity gradients for the York River and Chickahominy/James River estuaries were predicted for the three sea-level rise scenarios. When a 50-cm sea-level rise scenario on the York River during a typical year (2005) was used, the model simulation showed a salinity of 15 parts per thousand (ppt) at river kilometer (km) 39. During a dry year (2002), the same salinity (15 ppt) was simulated at river km 45, which means that saltwater was shown to migrate 6 km farther upstream during a dry year than a typical year. The same was true of the Chickahominy River for a 50-cm sea-level rise scenario but to a greater extent; a salinity of 4 ppt was simulated at river km 13 during a typical year and at river km 28 during a dry year, indicating that saltwater migrated 15 km farther upstream during a dry year. Near a drinking-water intake on the Chickahominy River, for a dry year, salinity is predicted to more than double for all three sea-level rise scenarios, relative to a typical year. During a typical year at this location, salinity is predicted to increase to 0.006, 0.07, and more than 2 ppt for the 30-, 50-, and 100-cm rise scenarios, respectively

Hospital ownership and financial performance: a quantitative research review

We apply meta-analytic methods to conduct a quantitative review of the empirical literature since 1999 comparing financial performance of US for-profit, not-for-profit, and government-owned general acute hospitals. We find that tthe diverse results in the hospital ownership literature can be explained largely by differences in authors' underlying theoretical frameworks, assumptions about the functional form of the dependent variables, and model specifications. Weaker methods and functional forms tend to predict larger differences in financial performance between not-for-profits and for-profits. The combined estimates across studies suggest little difference in cost among all three types of hospital ownership, and that for-profit hospitals generate more revenue and greater profits than not-for-prorfits hospitals, alhough the difference is only of modest economic significance. There is little difference in revenue or profits between government and not-for-profit hospitals

Hospital ownership and quality of care: what explains the different results?

Does quality of care systematically differ among government-owned, private not-for-profit, and for-profit hospitals? A large empirical literature provides conflicting evidance. Through quantitative review of 46 studies since 1990, we find that several study features that can explain divergent results: analytic methods, disease studied, and data sources. For unprofitable care, how studies handle market competition and regional differences account for substantial variation. Policymakers should be aware that differences in results appear to arise predominately from differences between studies' analytic methods. Moreover, conventional methods of meta-analysis synthesis should be applied with great caution given the considerable overlap among studied hospitals

Complete Mapping of Divergent Amino Acids Responsible for Differential Ligand Binding of Folate Receptors α and β

The folate receptor (FR) type alpha may be distinguished from FR-beta by its higher affinity for the circulating folate coenzyme, (6S)-5-methyltetrahydrofolate (5-CH3H4folate), and its opposite stereospecificity for reduced folate coenzymes. Previous studies showed that a single leucine to alanine substitution at position 49 of the mature protein sequence is responsible for the functional divergence of FR-beta (Shen, F., Zheng, X., Wang, H., and Ratnam, M. (1997) Biochemistry 36, 6157-6163); however, the results also indicated that the minimum requirement for conversion of FR-beta to the functional equivalent of FR-alpha should include amino acid substitution(s) downstream of residue 92 in addition to mutation of L49A. To pinpoint those residues, chimeric FR-betaL49A/FR-alpha constructs including progressively shorter segments of FR-alpha downstream of position 92 as well as selected point mutants were studied. Simultaneous substitution of Leu-49, Phe-104, and Gly-166 in FR-beta with the corresponding FR-alpha residues Ala, Val, and Glu, respectively, reconstituted the ligand binding characteristics of FR-alpha. The results also exclude a role for other residues in FR-alpha in determining its functional divergence. A homology model of FR-alpha based on the three-dimensional structure of the chicken riboflavin-binding protein is used to show the position of residues 49, 104, and 166 in relation to the hydrophobic cleft corresponding to the riboflavin-binding pocket

Hospital ownership and quality of care: what explains the different results?

Does quality of care systematically differ among government-owned, private not-for-profit, and for-profit hospitals? A large empirical literature provides conflicting evidance. Through quantitative review of 46 studies since 1990, we find that several study features that can explain divergent results: analytic methods, disease studied, and data sources. For unprofitable care, how studies handle market competition and regional differences account for substantial variation. Policymakers should be aware that differences in results appear to arise predominately from differences between studies' analytic methods. Moreover, conventional methods of meta-analysis synthesis should be applied with great caution given the considerable overlap among studied hospitals

Electron slingshot acceleration in relativistic preturbulent shocks explored via emitted photon polarization

Transient electron dynamics near the interface of counterstreaming plasmas at the onset of a relativistic collisionless shock (RCS) is investigated using particle-in-cell simulations. We identify a slingshot-like injection process induced by the drifting electric field sustained by the flowing focus of backwards-moving electrons, which is distinct from the well-known stochastic acceleration. The flowing focus signifies the plasma kinetic transition from a preturbulent laminar motion to a chaotic turbulence. We find a characteristic correlation between the electron dynamics in the slingshot acceleration and the photon emission features. In particular, the integrated radiation from the RCS exhibits a counterintuitive non-monotonic dependence of the photon polarization degree on the photon energy, which originates from a polarization degradation of relatively high-energy photons emitted by the slingshot-injected electrons. Our results demonstrate the potential of photon polarization as an essential information source in exploring intricate transient dynamics in RCSs with relevance for earth-based plasma and astrophysical scenarios.Comment: 8 pages, 5 figure

Novel plasmid-mediated colistin resistance gene mcr-3 in Escherichia coli

The mobile colistin resistance gene mcr-1 has attracted global attention, as it heralds the breach of polymyxins, one of the last-resort antibiotics for the treatment of severe clinical infections caused by multidrug-resistant Gramnegative bacteria. To date, six slightly different variants of mcr-1, and a second mobile colistin resistance gene, mcr-2, have been reported or annotated in the GenBank database. Here, we characterized a third mobile colistin resistance gene, mcr-3. The gene coexisted with 18 additional resistance determinants in the 261-kb IncHI2-type plasmid pWJ1 from porcine Escherichia coli. mcr-3 showed 45.0% and 47.0% nucleotide sequence identity to mcr-1 and mcr-2, respectively, while the deduced amino acid sequence of MCR-3 showed 99.8 to 100% and 75.6 to 94.8% identity to phosphoethanolamine transferases found in other Enterobacteriaceae species and in 10 Aeromonas species, respectively. pWJ1 was mobilized to an E. coli recipient by conjugation and contained a plasmid backbone similar to those of other mcr- 1-carrying plasmids, such as pHNSHP45-2 from the original mcr-1-harboring E. coli strain. Moreover, a truncated transposon element, TnAs2, which was characterized only in Aeromonas salmonicida, was located upstream of mcr-3 in pWJ1. This ΔTnAs2-mcr-3 element was also identified in a shotgun genome sequence of a porcine E. coli isolate from Malaysia, a human Klebsiella pneumoniae isolate from Thailand, and a human Salmonella enterica serovar Typhimurium isolate from the United States. These results suggest the likelihood of a wide dissemination of the novel mobile colistin resistance gene mcr-3 among Enterobacteriaceae and aeromonads; the latter may act as a potential reservoir for mcr-3. IMPORTANCE The emergence of the plasmid-mediated colistin resistance gene mcr-1 has attracted substantial attention worldwide. Here, we examined a colistin-resistant Escherichia coli isolate that was negative for both mcr-1 and mcr-2 and discovered a novel mobile colistin resistance gene, mcr-3. The amino acid sequence of MCR-3 aligned closely with phosphoethanolamine transferases from Enterobacteriaceae and Aeromonas species originating from both clinical infections and environmental samples collected in 12 countries on four continents. Due to the ubiquitous profile of aeromonads in the environment and the potential transfer of mcr-3 between Enterobacteriaceae and Aeromonas species, the wide spread of mcr-3 may be largely underestimated. As colistin has been and still is widely used in veterinary medicine and used at increasing frequencies in human medicine, the continuous monitoring of mobile colistin resistance determinants in colistin-resistant Gram-negative bacteria is imperative for understanding and tackling the dissemination of mcr genes in both the agricultural and health care sectors

Tenotomy-induced muscle atrophy is sex-specific and independent of NFκB

The nuclear factor-κB (NFκB) pathway is a major thoroughfare for skeletal muscle atrophy and is driven by diverse stimuli. Targeted inhibition of NFκB through its canonical mediator IKKβ effectively mitigates loss of muscle mass across many conditions, from denervation to unloading to cancer. In this study, we used gain- and loss-of-function mouse models to examine the role of NFκB in muscle atrophy following rotator cuff tenotomy - a model of chronic rotator cuff tear. IKKβ was knocked down or constitutively activated in muscle-specific inducible transgenic mice to elicit a twofold gain or loss of NFκB signaling. Surprisingly, neither knockdown of IKKβ nor overexpression of caIKKβ significantly altered the loss of muscle mass following tenotomy. This finding was consistent across measures of morphological adaptation (fiber cross-sectional area, fiber length, fiber number), tissue pathology (fibrosis and fatty infiltration), and intracellular signaling (ubiquitin-proteasome, autophagy). Intriguingly, late-stage tenotomy-induced atrophy was exacerbated in male mice compared with female mice. This sex specificity was driven by ongoing decreases in fiber cross-sectional area, which paralleled the accumulation of large autophagic vesicles in male, but not female muscle. These findings suggest that tenotomy-induced atrophy is not dependent on NFκB and instead may be regulated by autophagy in a sex-specific manner