Effectiveness of an Interprofessional Education Event for Graduate Health Professional Students

ABSTRACT Purpose: The purpose of this study was to investigate the impact of a single, optional, half-day, interprofessional education (IPE) event for a myriad of graduate-level health professional students (n=44) at a university in Illinois, USA. Methods: The researchers in this study examined students’ performance on two out of six of the domains on the Interprofessiomnal Collaborator Assessment Rubric (ICAR): Roles and Responsibilities and Communication Strategies. This study also investigated quantitative and qualitative findings related to student perceptions regarding this IPE opportunity. Results: Results indicated that students met or exceeded the minimum competency for the ranking of “developing” for all 6 of the behaviors evaluated. Results also revealed that this half-day extracurricuricular IPE event was viewed favorably by health-professional students and created a venue whereby students belonging to different health professional programs can enter into discussions and learn about each others’ respective roles and responsibilities in patient care. Conclusion: The creation and implementation of short term extracurricular IPE events may be a valuable alternative for healthcare programs that are unable to implement IPE activities due to some of the common barriers impacting the development, implementation, or continuation of IPE opportunities

Electron and hole states in quantum-dot quantum wells within a spherical 8-band model

In order to study heterostructures composed both of materials with strongly different parameters and of materials with narrow band gaps, we have developed an approach, which combines the spherical 8-band effective-mass Hamiltonian and the Burt's envelope function representation. Using this method, electron and hole states are calculated in CdS/HgS/CdS/H_2O and CdTe/HgTe/CdTe/H_2O quantum-dot quantum-well heterostructures. Radial components of the wave functions of the lowest S and P electron and hole states in typical quantum-dot quantum wells (QDQWs) are presented as a function of radius. The 6-band-hole components of the radial wave functions of an electron in the 8-band model have amplitudes comparable with the amplitude of the corresponding 2-band-electron component. This is a consequence of the coupling between the conduction and valence bands, which gives a strong nonparabolicity of the conduction band. At the same time, the 2-band-electron component of the radial wave functions of a hole in the 8-band model is small compared with the amplitudes of the corresponding 6-band-hole components. It is shown that in the CdS/HgS/CdS/H_2O QDQW holes in the lowest states are strongly localized in the well region (HgS). On the contrary, electrons in this QDQW and both electron and holes in the CdTe/HgTe/CdTe/H_2O QDQW are distributed through the entire dot. The importance of the developed theory for QDQWs is proven by the fact that in contrast to our rigorous 8-band model, there appear spurious states within the commonly used symmetrized 8-band model.Comment: 15 pages, 5 figures, E-mail addresses: [email protected], [email protected]

Development of an eight-band theory for quantum-dot heterostructures

We derive a nonsymmetrized 8-band effective-mass Hamiltonian for quantum-dot heterostructures (QDHs) in Burt's envelope-function representation. The 8x8 radial Hamiltonian and the boundary conditions for the Schroedinger equation are obtained for spherical QDHs. Boundary conditions for symmetrized and nonsymmetrized radial Hamiltonians are compared with each other and with connection rules that are commonly used to match the wave functions found from the bulk kp Hamiltonians of two adjacent materials. Electron and hole energy spectra in three spherical QDHs: HgS/CdS, InAs/GaAs, and GaAs/AlAs are calculated as a function of the quantum dot radius within the approximate symmetrized and exact nonsymmetrized 8x8 models. The parameters of dissymmetry are shown to influence the energy levels and the wave functions of an electron and a hole and, consequently, the energies of both intraband and interband transitions.Comment: 36 pages, 10 figures, E-mail addresses: [email protected], [email protected]

On "Dotsenko-Fateev" representation of the toric conformal blocks

We demonstrate that the recent ansatz of arXiv:1009.5553, inspired by the original remark due to R.Dijkgraaf and C.Vafa, reproduces the toric conformal blocks in the same sense that the spherical blocks are given by the integral representation of arXiv:1001.0563 with a peculiar choice of open integration contours for screening insertions. In other words, we provide some evidence that the toric conformal blocks are reproduced by appropriate beta-ensembles not only in the large-N limit, but also at finite N. The check is explicitly performed at the first two levels for the 1-point toric functions. Generalizations to higher genera are briefly discussed.Comment: 10 page

Selberg Supertrace Formula for Super Riemann Surfaces III: Bordered Super Riemann Surfaces

This paper is the third in a sequel to develop a super-analogue of the classical Selberg trace formula, the Selberg supertrace formula. It deals with bordered super Riemann surfaces. The theory of bordered super Riemann surfaces is outlined, and the corresponding Selberg supertrace formula is developed. The analytic properties of the Selberg super zeta-functions on bordered super Riemann surfaces are discussed, and super-determinants of Dirac-Laplace operators on bordered super Riemann surfaces are calculated in terms of Selberg super zeta-functions.Comment: 43 pages, amste

N-Terminal Arginines Modulate Plasma-Membrane Localization of Kv7.1/KCNE1 Channel Complexes

BACKGROUND AND OBJECTIVE: The slow delayed rectifier current (I(Ks)) is important for cardiac action potential termination. The underlying channel is composed of Kv7.1 α-subunits and KCNE1 β-subunits. While most evidence suggests a role of KCNE1 transmembrane domain and C-terminus for the interaction, the N-terminal KCNE1 polymorphism 38G is associated with reduced I(Ks) and atrial fibrillation (a human arrhythmia). Structure-function relationship of the KCNE1 N-terminus for I(Ks) modulation is poorly understood and was subject of this study. METHODS: We studied N-terminal KCNE1 constructs disrupting structurally important positively charged amino-acids (arginines) at positions 32, 33, 36 as well as KCNE1 constructs that modify position 38 including an N-terminal truncation mutation. Experimental procedures included molecular cloning, patch-clamp recording, protein biochemistry, real-time-PCR and confocal microscopy. RESULTS: All KCNE1 constructs physically interacted with Kv7.1. I(Ks) resulting from co-expression of Kv7.1 with non-atrial fibrillation '38S' was greater than with any other construct. Ionic currents resulting from co-transfection of a KCNE1 mutant with arginine substitutions ('38G-3xA') were comparable to currents evoked from cells transfected with an N-terminally truncated KCNE1-construct ('Δ1-38'). Western-blots from plasma-membrane preparations and confocal images consistently showed a greater amount of Kv7.1 protein at the plasma-membrane in cells co-transfected with the non-atrial fibrillation KCNE1-38S than with any other construct. CONCLUSIONS: The results of our study indicate that N-terminal arginines in positions 32, 33, 36 of KCNE1 are important for reconstitution of I(Ks). Furthermore, our results hint towards a role of these N-terminal amino-acids in membrane representation of the delayed rectifier channel complex

Nicotine exploits a COPI-mediated process for chaperone-mediated up-regulation of its receptors

Chronic exposure to nicotine up-regulates high sensitivity nicotinic acetylcholine receptors (nAChRs) in the brain. This up-regulation partially underlies addiction and may also contribute to protection against Parkinson’s disease. nAChRs containing the α6 subunit (α6* nAChRs) are expressed in neurons in several brain regions, but comparatively little is known about the effect of chronic nicotine on these nAChRs. We report here that nicotine up-regulates α6* nAChRs in several mouse brain regions (substantia nigra pars compacta, ventral tegmental area, medial habenula, and superior colliculus) and in neuroblastoma 2a cells. We present evidence that a coat protein complex I (COPI)-mediated process mediates this up-regulation of α6* or α4* nAChRs but does not participate in basal trafficking. We show that α6β2β3 nAChR up-regulation is prevented by mutating a putative COPI-binding motif in the β3 subunit or by inhibiting COPI. Similarly, a COPI-dependent process is required for up-regulation of α4β2 nAChRs by chronic nicotine but not for basal trafficking. Mutation of the putative COPI-binding motif or inhibition of COPI also results in reduced normalized Förster resonance energy transfer between α6β2β3 nAChRs and εCOP subunits. The discovery that nicotine exploits a COPI-dependent process to chaperone high sensitivity nAChRs is novel and suggests that this may be a common mechanism in the up-regulation of nAChRs in response to chronic nicotine

Corticosterone Alters AMPAR Mobility and Facilitates Bidirectional Synaptic Plasticity

Background: The stress hormone corticosterone has the ability both to enhance and suppress synaptic plasticity and learning and memory processes. However, until today there is very little known about the molecular mechanism that underlies the bidirectional effects of stress and corticosteroid hormones on synaptic efficacy and learning and memory processes. In this study we investigate the relationship between corticosterone and AMPA receptors which play a critical role in activity-dependent plasticity and hippocampal-dependent learning. Methodology/Principal Findings: Using immunocytochemistry and live cell imaging techniques we show that corticosterone selectively increases surface expression of the AMPAR subunit GluR2 in primary hippocampal cultures via a glucocorticoid receptor and protein synthesis dependent mechanism. In agreement, we report that corticosterone also dramatically increases the fraction of surface expressed GluR2 that undergo lateral diffusion. Furthermore, our data indicate that corticosterone facilitates NMDAR-invoked endocytosis of both synaptic and extra-synaptic GluR2 under conditions that weaken synaptic transmission. Conclusion/Significance: Our results reveal that corticosterone increases mobile GluR2 containing AMPARs. The enhanced lateral diffusion properties can both facilitate the recruitment of AMPARs but under appropriate conditions facilitate the loss of synaptic AMPARs (LTD). These actions may underlie both the facilitating and suppressive effects of corticosteroid hormones on synaptic plasticity and learning and memory and suggest that these hormones accentuate synaptic efficacy