An Analysis of Data Regarding Public Private Partnerships to Encourage Hotel Development in the United States

In recent decades, communities in the United States have increasingly turned to public private partnerships, also known as PPPs or P3s, to encourage development of large convention headquarter hotels. Under such arrangements communities provide incentives to encourage private sector investors to build hotels that can house delegates, exhibitors and other attendees participating in events at publicly owned conventions centers. In recent years the practice of public subsidies, and in some cases outright public ownership, has spread beyond convention hotels to a wide range of hotel projects. This study presents data collected on these publicly assisted hotels to provide a picture of how these arrangements are structured. It goes on propose an economic model based on the income capitalization approach to valuation to determine the rate of return that communities can expect from their investments in these project

The Impact of Publicly Owned Hotels on Competing Properties

Substantial public subsidies, and even outright public ownership, of hotels have become common in the United States as communities target tourism as an integral economic development tool. A critical question that is increasingly being raised about the public sector entering the hotel business is, are these government-funded facilities unfair competition to properties developed by the private sector? The common reply to these concerns is that the publicly owned hotel is critical to growing demand for lodging accommodation and that once it opens, the new hotel will attract enough new business that all hotels will benefit. We use an event study to test this hypothesis across all of the 100% publicly developed hotels for which there are sufficient data to conduct the analysis. In looking at these 21 hotels, we found strong evidence that the performance of neighboring hotels worsens after the introduction of a publicly owned hotel

The Impact of Publicly Subsidized Hotels in the United States on Competing Properties

This paper examines the use of publicly funded subsidies to encourage hotel development in the United States. It reports highlights from the largest and most complete data base assembled on these transactions. This data shows that public subsidies play a significant role in American hotel development and many projects that are in various stages of the development pipeline include the use of public funds. It goes on to present eight impact analyses that look at how key performance metrics of competing hotels in various markets are affected when they have to contend with new entrants that are subsidized. Three markets saw increases in indexed RevPAR, while in the other five markets competing hotels seemed to suffer after the introduction of publicly subsidized competition

Correspondence : In support of the IES method of evaluating light source colour rendition

Version of RecordPublishe

Long-term correction of diabetes in rats after lentiviral hepatic insulin gene therapy

Aims/hypothesis: Type 1 diabetes results from the autoimmune destruction of pancreatic beta cells. Exogenous insulin therapy cannot achieve precise physiological control of blood glucose concentrations, and debilitating complications develop. Lentiviral vectors are promising tools for liver-directed gene therapy. However, to date, transduction rates in vivo remain low in hepatocytes, without the induction of cell cycling. We investigated long-term transgene expression in quiescent hepatocytes in vitro and determined whether the lentiviral delivery of furin-cleavable insulin to the liver could reverse diabetes in rats. Materials and methods: To improve transduction efficiency in vitro, we optimised hepatocyte isolation and maintenance protocols and, using an improved surgical delivery method, delivered furin-cleavable insulin alone or empty vector to the livers of streptozotocin-induced diabetic rats by means of a lentiviral vector. Rats were monitored for changes in body weight and blood glucose, and intravenous glucose tolerance tests were performed. Expression of insulin was determined by RT-PCR, immunohistochemistry and electron microscopy. Results: We achieved long-term transgene expression in quiescent hepatocytes in vitro (87 ± 1.2% transduction efficiency), with up to 60 ± 3.2% transduction in vivo. We normalised blood glucose for 500 days-a significantly longer period than previously reported-making this the first successful study using a lentiviral vector. This procedure resulted in the expression of genes encoding several beta cell transcription factors, some pancreatic endocrine transdifferentiation, hepatic insulin storage in granules, and restoration of glucose tolerance. Liver function tests remained normal. Importantly, pancreatic exocrine transdifferentiation did not occur. Conclusions/interpretation: Our data suggest that this regimen may ultimately be employed for the treatment of type 1 diabetes

Glucose Transporter 1 and Monocarboxylate Transporters 1, 2, and 4 Localization within the Glial Cells of Shark Blood-Brain-Barriers

Although previous studies showed that glucose is used to support the metabolic activity of the cartilaginous fish brain, the distribution and expression levels of glucose transporter (GLUT) isoforms remained undetermined. Optic/ultrastructural immunohistochemistry approaches were used to determine the expression of GLUT1 in the glial blood-brain barrier (gBBB). GLUT1 was observed solely in glial cells; it was primarily located in end-feet processes of the gBBB. Western blot analysis showed a protein with a molecular mass of 50 kDa, and partial sequencing confirmed GLUT1 identity. Similar approaches were used to demonstrate increased GLUT1 polarization to both apical and basolateral membranes in choroid plexus epithelial cells. To explore monocarboxylate transporter (MCT) involvement in shark brain metabolism, the expression of MCTs was analyzed. MCT1, 2 and 4 were expressed in endothelial cells; however, only MCT1 and MCT4 were present in glial cells. In neurons, MCT2 was localized at the cell membrane whereas MCT1 was detected within mitochondria. Previous studies demonstrated that hypoxia modified GLUT and MCT expression in mammalian brain cells, which was mediated by the transcription factor, hypoxia inducible factor-1. Similarly, we observed that hypoxia modified MCT1 cellular distribution and MCT4 expression in shark telencephalic area and brain stem, confirming the role of these transporters in hypoxia adaptation. Finally, using three-dimensional ultrastructural microscopy, the interaction between glial end-feet and leaky blood vessels of shark brain was assessed in the present study. These data suggested that the brains of shark may take up glucose from blood using a different mechanism than that used by mammalian brains, which may induce astrocyte-neuron lactate shuttling and metabolic coupling as observed in mammalian brain. Our data suggested that the structural conditions and expression patterns of GLUT1, MCT1, MCT2 and MCT4 in shark brain may establish the molecular foundation of metabolic coupling between glia and neurons

Assessing EM Patient Safety and Quality Improvement Milestones Using a Novel Debate Format

Graduate medical education is increasingly focused on patient safety and quality improvement; training programs must adapt their curriculum to address these changes. We propose a novel curriculum for emergency medicine (EM) residency training programs specifically addressing patient safety, systems-based management, and practice-based performance improvement, called “EM Debates.” Following implementation of this educational curriculum, we performed a cross-sectional study to evaluate the curriculum through resident self-assessment. Additionally, a cross-sectional study to determine the ED clinical competency committee’s (CCC) ability to assess residents on specific competencies was performed. Residents were overall very positive towards the implementation of the debates. Of those participating in a debate, 71% felt that it improved their individual performance within a specific topic, and 100% of those that led a debate felt that they could propose an evidence-based approach to a specific topic. The CCC found that it was easier to assess milestones in patient safety, systems-based management, and practice-based performance improvement (sub-competencies 16, 17, and 19) compared to prior to the implementation of the debates. The debates have been a helpful venue to teach EM residents about patient safety concepts, identifying medical errors, and process improvement

Tolbutamide causes open channel blockade of cystic fibrosis transmembrane conductance regulator Cl- channels.

Cystic fibrosis transmembrane conductance regulator (CFTR) is an epithelial Cl- channel that is regulated by protein kinase A and cytosolic nucleotides. Previously, Sheppard and Welsh reported that the sulfonylureas glibenclamide and tolbutamide reduced CFTR whole cell currents. The aim of this study was to quantify the effects of tolbutamide on CFTR gating in excised membrane patches containing multiple channels. We chose tolbutamide because weak (i.e., fast-type) open channel blockers introduce brief events into multichannel recordings that can be readily quantified by current fluctuation analysis. Inspection of current records revealed that the addition of tolbutamide reduced the apparent single-channel current amplitude and increased the open-channel noise, as expected for a fast-type open channel blocker. The apparent decrease in unitary current amplitude provides a measure of open probability within a burst (P0 Burst), and the resulting concentration-response relationship was described by a simple Michaelis-Menten inhibition function. The concentration of tolbutamide causing a 50% reduction of Po Burst (540 +/- 20 microM) was similar to the concentration producing a 50% inhibition of short-circuit current across T84 colonic epithelial cell monolayers (400 +/- 20 microM). Changes in CFTR gating were then quantified by analyzing current fluctuations. Tolbutamide caused a high-frequency Lorentzian (corner frequency, fc > 300 Hz) to appear in the power density spectrum. The fc of this Lorentzian component increased as a linear function of tolbutamide concentration, as expected for a pseudo-first-order open-blocked mechanism and yielded estimates of the on rate (koff = 2.8 +/- 0.3 microM-1 s-1), the off rate (kon = 1210 +/- 225 s-1), and the dissociation constant (KD = 430 +/- 80 microM). Based on these observations, we propose that there is a bimolecular interaction between tolbutamide and CFTR, causing open channel blockade