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Johnson County Hospital was a hospital located in Mountain City, TN that existed from 1972 until its final closure in 1998. The hospital faced multiple financial challenges during its existence and was forced to close three times. In 1988 it closed for the penultimate time, and as it had in the past, it counted on the community, local business and local government to reopen the hospital. Three local businessmen were particularly dedicated to reopening the county hospital and reached out to East Tennessee State University (ETSU) and their newly formed College of Medicine. A partnership was formed between the community and ETSU to open a rural campus to educate medical, nursing, public health and allied health students. This rural campus was made a reality through the Kellogg Grant awarded to ETSU in 1991 and was expanded to include graduate medical education in 1996. This collaboration between the community, local businesses, local government and ETSU was able to reopen the hospital in 1992 and jump-started interprofessional education at ETSU which is continued today in the form of the Academic Health Sciences Center and the Interprofessional Education Program.

Experiments were performed to characterize hydraulic jumps that form due to liquid jet impingement on superhydrophobic surfaces with alternating micro-ribs and cavities. If the surface is unimmersed, a surface tension based transition into droplets occurs, so a known depth of water was imposed downstream from the hydraulic jump to ensure the existence of a hydraulic jump. The surfaces are characterized by the cavity fraction, which is defined as the width of a cavity divided by the combined width of a cavity and an adjoining rib. Four different surface designs were studied, with respective cavity fractions of 0 (smooth surface), 0.5, 0.8, and 0.93. Each surface was tested in its naturally hydrophilic state where water was allowed to flood the cavities, as well as with a hydrophobic coating which prevented water from entering the cavities and created a liquid-gas interface over much of the surface. The experimental data spans a Weber number range (based on the jet velocity and radius) of 3x102 to 1.05x103 and a corresponding Reynolds number range of 1.15x104 to 2.14x104. While smooth surfaces always result in circular transitions, for any rib and cavity patterned surface the flow exhibits a nearly elliptical transition from the thin film, where the major axis of the ellipse is parallel to the ribs, concomitant with greater slip in that direction. When the downstream depth is small and a superhydrophobic surface is used, the water is completely expelled from the surface, and the thin film breaks up into droplets due to surface tension interactions. When the downstream depth is large or the surface is hydrophilic a hydraulic jump exists. When the water depth downstream of the jump increases, the major and minor axis of the jump decreases due to an increase in hydrostatic force, following classical hydraulic jump behavior. The experimental results indicate that for a given cavity fraction and downstream depth, the radius of the jump increases with increasing Reynolds number. The jump radius perpendicular to the ribs is notably less than that for a smooth surface, and this radius decreases with increasing cavity fraction. When comparing flow over superhydrophobic (coated) surfaces to patterned, hydrophilic (uncoated) surfaces, a general increase is seen in the radial location of the hydraulic jump in the direction of the ribs, while no statistically significant change is seen in the direction perpendicular to the ribs.

BACKGROUND: Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN) is the most severe form of cutaneous adverse drug reaction and is characterized by extensive epidermal destruction of the skin and mucosal surfaces. Controversy remains regarding the immunopathogenesis of the disease. It has long been assumed that CD8 cytotoxic T cells mediate cell death by releasing cytotoxic granules and soluble granulysin that trigger keratinocyte apoptosis. However, this does not explain the massive cell death or inflammation that is observed clinically. We have preliminary evidence from transcriptional profiling of patient skin samples suggesting that the cell death pathways necroptosis and pyroptosis may mediate SJS/TEN. Herein we utilize retrospectively and prospectively collected patient samples to investigate these cell death pathways. OBJECTIVE: The goals of this study are two-fold: (i) to investigate cell death pathways in retrospectively-collected (SJS/TEN) patient skin samples and (ii) to directly test the cell death mediators and pathways mediating SJS/TEN using a novel in vitro model. METHODS: Clinically and histopathologically confirmed SJS/TEN skin specimens and control skin specimens from non-blistering T cell mediated drug reactions and healthy skin were obtained following retrospective analysis from a multi-centered patient database. Gene expression profiling is being performed using the NanoString nCounter® System on these samples as a second patient cohort to confirm and expand on preliminary study findings. In parallel, we have optimized the use of a novel human skin platform for an in vitro model of SJS/TEN. We also collected human serum from a prospective study of SJS/TEN and control patients and have optimized and are actively collecting blister fluid from SJS/TEN and control patients in an ongoing prospective study for use in this model. RESULTS: Through an extensive pathology database and medical record search of potential cases at Brigham and Women's Hospital, we identified a second patient cohort of SJS/TEN, non-blistering delayed-type drug hypersensitivity reactions and healthy controls. We identified and are collecting thorough demographic, clinical and laboratory data on 61 potential candidates for SJS/TEN, 4 for Drug Reaction with Eosinophilia Syndrome (DRESS), and 200 for Morbilliform Drug Eruptions (MDE). This second cohort is in the final step of analysis with review by an expert clinician to confirm cases. In parallel, we have designed an expansive gene panel to confirm cell death mediator and marker transcription in our bank of skin samples. This 815 gene panel uses the pre-designed panel from Nanostring®, spiked with an additional 30 genes specific to apoptosis, pyroptosis, and necroptosis. We reviewed multiple potential in vitro skin models and identified GenoSkin® as the most suitable human skin platform for our in vitro model. We collected serum from 6 SJS/TEN patients and 6 non-blistering drug reaction patients and 3 healthy controls, and are actively collecting blister fluid from SJS/TEN and thermal burn control patients for analysis in this model. CONCLUSIONS: Our preliminary data suggest necroptosis and pyroptosis induced by soluble death mediators tumor necrosis factor (TNF) alpha and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as the main cell death pathways responsible for SJS/TEN. We have successfully identified a large number of potential patient samples of both cases and controls to perform transcriptional profiling using a self-designed gene panel to confirm and expand upon our preliminary data. We have successfully collected prospectively patient serum and are actively collecting patient blister fluid for analysis in an optimized in vitro model using GenoSkin®. SJS/TEN is severely understudied and lacks a standard protocol for care. This stems from uncertainty surrounding disease pathobiology. It is critical that we use innovative approaches to interrogate the mechanism mediating disease to advance the field, and, most importantly, to improve the quality of care for these patients.

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Increased accountability mandates from the No Child Left Behind Act of 2001 and the Individuals with Disabilities Education Improvement Act of 2004 have resulted in general education teachers with disabled students in their classrooms. Within the inclusive classroom, the special education teacher and the general education teacher must develop a collaborative relationship that will consider the needs of the special education students and general education students. Villa and Thousand (1996) described the benefits of collaboration in schools: “Collaboration enables school personnel to meet diverse student needs through shared expertise and ownership of problem definitions and solutions” (p. 170). The purpose of this qualitative case study was to examine how special education teachers and general education teachers in inclusive classrooms collaborate regarding the needs of students. The participants for this study were four special education teachers, four general education teachers, and the administrator in one elementary school located in Mississippi. The research questions for this study were derived from six defining characteristics of collaboration as described by Friend and Cook (1996). The six defining characteristics are: (a) collaboration is voluntary; (b) collaboration requires parity among participants; (c) collaboration is based on mutual goals; (d) collaboration depends on shared responsibility for participation and decision making; (e)collaboration requires individuals to share responsibility for outcomes. There were two research questions posed for this study: (1) How do special education teachers collaborate, as defined by Friend and Cook (1996), when working with general education teachers? (2) How do general education teachers collaborate, as defined by Friend and Cook (1996), when working with special education teachers?

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