The Development and Establishment of a Pre-School Music Therapy Program

The purpose of this study was to gain insight into how a music therapist can develop and establish a music therapy program in the school setting. An experienced Licensed Creative Arts Therapist and Board Certified-Music Therapist, who began a music therapy program, was the sole participant in this study. The participant was interviewed a total of three times. The researcher asked open-ended questions regarding the history of how the participant developed and maintains her current music therapy program. The literature regarding the topic is scant, suggesting the need for studies to be conducted regarding this topic. The researcher extricated themes that were found relevant in the participant’s recount of how the music therapy program was developed and established. These themes include advocacy, personality traits, funding, and roadblocks. Passion, advocacy, and articulation are themes that the researcher found to be most important when developing and establishing a music therapy program in the school setting

Water Security for Texas: A Post-Secondary Education Pathway for the Water Workforce

Water and wastewater industry leaders in Texas and throughout the United States have expressed concern over high rates of retirement eligibility and difficulties finding and attracting workers ready to fill job openings, especially for work in smaller systems. In late January 2018, the U.S. Government Accountability Office released a report on water workforce readiness and a bill was introduced in the U.S. Senate to establish a water infrastructure workforce development program. Concern over existing education of workers in water and demographic information projecting future workforce readiness are commonly cited as signaling a coming crisis for the water industry. An alignment of post-secondary training and industry needs is recommended to meet coming workforce employment requirements for Texas and the nation. A model post-secondary education pathway for water science and technology is described to support water workforce readiness

Mycophenolate Mofetil-Related Enterocolitis and Weight Loss: A Pediatric Case Series

Mycophenolate mofetil (MMF) is an immunosuppressive medication utilized in the management of both autoimmune and solid organ transplant patients. Diarrhea is a common gastrointestinal side effect of MMF, but more severe forms of GI symptoms are described in renal transplant patients with a distinct pattern of histopathologic change, similar to graft-versus-host disease or Crohn's disease. This rare entity, commonly referred to as “MMF-related enterocolitis,” has been described in adult patients, mostly in renal transplant patients, and in only two pediatric renal transplant patients. In previously reported cases, symptoms and abnormal histopathology improve with dose reduction of MMF. We describe a series of three pediatric patients with varied underlying disease process who presented with severe diarrhea and histopathologic findings characteristic of MMF-related enterocolitis, who share a novel finding of weight loss as a complication of MMF-related enterocolitis in pediatric patients

Specific Immunosuppression with Inducible Foxp3-Transduced Polyclonal T cells

Forkhead box p3 (Foxp3)-expressing regulatory T cells are key mediators of peripheral tolerance suppressing undesirable immune responses. Ectopic expression of Foxp3 confers regulatory T cell phenotype to conventional T cells, lending itself to therapeutic use in the prevention of autoimmunity and transplant rejection. Here, we show that adoptive transfer of polyclonal, wild-type T cells transduced with an inducible form of Foxp3 (iFoxp3) can be used to suppress immune responses on demand. In contrast to Foxp3-transduced cells, iFoxp3-transduced cells home “correctly” into secondary lymphoid organs, where they expand and participate in immune responses. Upon induction of iFoxp3, the cells assume regulatory T cell phenotype and start to suppress the response they initially partook in without causing systemic immunosuppression. We used this approach to suppress collagen-induced arthritis, in which conventional Foxp3-transduced cells failed to show any effect. This provides us with a generally applicable strategy to specifically halt immune responses on demand without prior knowledge of the antigens involved

Very Early Optical Afterglows of Gamma-Ray Bursts: Evidence for Relative Paucity of Detection

Very early observations with the Swift satellite of gamma-ray burst (GRB) afterglows reveal that the optical component is not detected in a large number of cases. This is in contrast to the bright optical flashes previously discovered in some GRBs (e.g. GRB 990123 and GRB 021211). Comparisons of the X-ray afterglow flux to the optical afterglow flux and prompt gamma-ray fluence is used to quantify the seemingly deficient optical, and in some cases X-ray, light at these early epochs. This comparison reveals that some of these bursts appear to have higher than normal gamma-ray efficiencies. We discuss possible mechanisms and their feasibility for explaining the apparent lack of early optical emission. The mechanisms considered include: foreground extinction, circumburst absorption, Ly-alpha blanketing and absorption due to high redshift, low density environments, rapid temporal decay, and intrinsic weakness of the reverse shock. Of these, foreground extinction, circumburst absorption, and high redshift provide the best explanations for most of the non-detections in our sample. There is tentative evidence of suppression of the strong reverse shock emission. This could be because of a Poynting-flux-dominated flow or a pure non-relativistic hydrodynamical reverse shock.Comment: 22 pages, 5 figures. Accepted for publication in Ap

Static Magnetic Field Exposure Reproduces Cellular Effects of the Parkinson's Disease Drug Candidate ZM241385

This study was inspired by coalescing evidence that magnetic therapy may be a viable treatment option for certain diseases. This premise is based on the ability of moderate strength fields (i.e., 0.1 to 1 Tesla) to alter the biophysical properties of lipid bilayers and in turn modulate cellular signaling pathways. In particular, previous results from our laboratory (Wang et al., BMC Genomics, 10, 356 (2009)) established that moderate strength static magnetic field (SMF) exposure altered cellular endpoints associated with neuronal function and differentiation. Building on this background, the current paper investigated SMF by focusing on the adenosine A(2A) receptor (A(2A)R) in the PC12 rat adrenal pheochromocytoma cell line that displays metabolic features of Parkinson's disease (PD).SMF reproduced several responses elicited by ZM241385, a selective A(2A)R antagonist, in PC12 cells including altered calcium flux, increased ATP levels, reduced cAMP levels, reduced nitric oxide production, reduced p44/42 MAPK phosphorylation, inhibited proliferation, and reduced iron uptake. SMF also counteracted several PD-relevant endpoints exacerbated by A(2A)R agonist CGS21680 in a manner similar to ZM241385; these include reduction of increased expression of A(2A)R, reversal of altered calcium efflux, dampening of increased adenosine production, reduction of enhanced proliferation and associated p44/42 MAPK phosphorylation, and inhibition of neurite outgrowth.When measured against multiple endpoints, SMF elicited qualitatively similar responses as ZM241385, a PD drug candidate. Provided that the in vitro results presented in this paper apply in vivo, SMF holds promise as an intriguing non-invasive approach to treat PD and potentially other neurological disorders

The genetics of neuropathic pain from model organisms to clinical application

Neuropathic pain (NeuP) arises due to injury of the somatosensory nervous system and is both common and disabling, rendering an urgent need for non-addictive, effective new therapies. Given the high evolutionary conservation of pain, investigative approaches from Drosophila mutagenesis to human Mendelian genetics have aided our understanding of the maladaptive plasticity underlying NeuP. Successes include the identification of ion channel variants causing hyper-excitability and the importance of neuro-immune signaling. Recent developments encompass improved sensory phenotyping in animal models and patients, brain imaging, and electrophysiology-based pain biomarkers, the collection of large well-phenotyped population cohorts, neurons derived from patient stem cells, and high-precision CRISPR generated genetic editing. We will discuss how to harness these resources to understand the pathophysiological drivers of NeuP, define its relationship with comorbidities such as anxiety, depression, and sleep disorders, and explore how to apply these findings to the prediction, diagnosis, and treatment of NeuP in the clinic