64 research outputs found

    Use of a Standardized Tracheostomy Patient Simulation to Evaluate Student Clinical Communication Skills

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    Simulation is a valid pedagogical tool used to teach students, observe student clinical skills, and to assess clinical competencies. During the COVID-19 pandemic, a lack of medical speech-language pathology placements required graduate programs to re-examine clinical training. Simulation has proven useful in providing an alternative and safe learning modality. Standardized patients, which are one simulation modality, provide increased standardization and higher fidelity than medical manikins. This is particularly true in the context of both student learning and demonstration of clinical communication skills (CCS) within a simulated learning environment where the simulated patient can interact authentically with the student clinician. CCS are important because they can lead to better treatment outcomes and strengthen the therapeutic alliance. The purpose of this study was to evaluate the evidence for a CCS training in the context of a speaking valve trial with a standardized tracheostomy patient. Results showed that students are demonstrating emerging skills or have already developed CCS in this context. Student questionnaire ratings suggest that this simulation was helpful to their learning as it provided a safe environment for them to practice valuable clinical skills. Simulation appears to be a viable modality to use when training CSD students to improve their CCS

    Boosting Confidence in Hearing Loss Services Through an Interprofessional Simulation led by Peer Instructors

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    Speech-language pathologists have an ethical responsibility to work with clients with hearing loss. Therefore, speech-language pathology (SLP) students must receive specific education and training in working with this population. SLP students may have low self-efficacy about their ability to work with clients with hearing loss if they haven’t participated in specific training. Interprofessional education utilizing peer teaching by doctor of audiology (AuD) students is one method for helping SLP students learn specific skills to address hearing loss in a clinical setting. The purpose of this study was to investigate SLP graduate students\u27 self-efficacy with working with individuals with hearing loss; SLP student perception of an interprofessional, peer-taught, experiential learning day (ELD) focused on skills related to serving individuals with hearing loss; and AuD peer teacher experiences. The ELD focused on developing skills and knowledge related to the insertion, troubleshooting, and maintenance of hearing aids. It also involved the exploration of hearing assistive technology, as well as information on hearing aids and hearing protection. The learning experience included multiple stations utilizing simulation, experiential learning, and AuD peer teaching. Results from this investigation suggest that an ELD benefits both SLP and AuD students. Specifically, SLP students reported increased self-efficacy for all tasks practiced, and AuD peer teachers reported increased confidence with teaching and a desire to teach again. Student questionnaire ratings suggested that SLP students enjoyed learning from AuD peer teachers, felt the ELD was beneficial to their learning, and thought they were gaining crucial skills for future practice. It appears that using an ELD with AuD peer teachers is a beneficial way to teach SLP students skills for working with clients with hearing loss

    Exploring the Role of Mental Toughness in Bone Mineral Content: A Preliminary Study

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    Bone mineral content (BMC), a measure of the mineral content within a person’s bones, is an important parameter in the assessment of bone health. Changes in BMC can be indicative of bone-related conditions. Dual-energy X-ray absorptiometry (DXA) is one of the most widely used and accurate methods for measuring BMC. Sex, age, race, and BMI are known to influence BMC. Physical activity is positively related to BMC levels. Mental toughness (MT) is conceptualized as a state-like psychological resource conducive to goal-oriented pursuits and is positively linked to physical activity outcomes. The relationship between MT and BMC has not been explored. PURPOSE: To investigate the isolated effect of MT on BMC after eliminating the confounding effects of sex, age, race, and BMI. METHODS: A total of 95 individuals participated in the study across two study sites. The sample (Mage = 34.57, SD = 15.87) was predominantly White (64%), normal weight/overweight (MBMI = 25.96, SD = 4.88) males (54%). DXA scans were performed on calibrated scanners using standard procedures. MT was assessed via the Mental Toughness Index (MTI). To reduce measurement error, the MTI was administered twice, separated by a two-week interval. A linear regression model was used to analyze the relationship between BMC and the average of the two MTI scores, while controlling for sex, age, race, and BMI in MATLAB (R2023a). A Cohen’s d for MT and BMC was additionally conducted. RESULTS: The linear regression model was BMC ~ 1 + Sex + Age + Race + BMI + MT. The overall regression was statistically significant (R2 = 0.183, F(94, 88) = 2.78, p = .012). MT was found to significantly predict BMC (ÎČ = 0.093, p = .008, d = 2.7). CONCLUSION: The findings underscore the statistical significance of MT as a predictor of BMC, even when accounting for the influence of sex, age, race, and BMI. The effect size points to the practical significance of this relationship, suggesting that individuals with higher MT levels may exhibit greater BMC. Future investigations should consider incorporating demographic covariates to gain deeper insights into these relationships and conduct interventional studies to identify potential underlying mechanisms (e.g., how trainable MT could be linked, to some degree, with an increase in BMC)

    Research and Education in Computational Science and Engineering

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    Over the past two decades the field of computational science and engineering (CSE) has penetrated both basic and applied research in academia, industry, and laboratories to advance discovery, optimize systems, support decision-makers, and educate the scientific and engineering workforce. Informed by centuries of theory and experiment, CSE performs computational experiments to answer questions that neither theory nor experiment alone is equipped to answer. CSE provides scientists and engineers of all persuasions with algorithmic inventions and software systems that transcend disciplines and scales. Carried on a wave of digital technology, CSE brings the power of parallelism to bear on troves of data. Mathematics-based advanced computing has become a prevalent means of discovery and innovation in essentially all areas of science, engineering, technology, and society; and the CSE community is at the core of this transformation. However, a combination of disruptive developments---including the architectural complexity of extreme-scale computing, the data revolution that engulfs the planet, and the specialization required to follow the applications to new frontiers---is redefining the scope and reach of the CSE endeavor. This report describes the rapid expansion of CSE and the challenges to sustaining its bold advances. The report also presents strategies and directions for CSE research and education for the next decade.Comment: Major revision, to appear in SIAM Revie

    Heterogeneity of cellular inflammatory responses in ageing white matter and relationship to Alzheimer’s and small vessel disease pathologies

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    Abstract: White matter lesions (WML) are common in the ageing brain, often arising in a field effect of diffuse white matter abnormality. Although WML are associated with cerebral small vessel disease (SVD) and Alzheimer’s disease (AD), their cause and pathogenesis remain unclear. The current study tested the hypothesis that different patterns of neuroinflammation are associated with SVD compared to AD neuropathology by assessing the immunoreactive profile of the microglial (CD68, IBA1 and MHC‐II) and astrocyte (GFAP) markers in ageing parietal white matter (PARWM) obtained from the Cognitive Function and Ageing Study (CFAS), an ageing population‐representative neuropathology cohort. Glial responses varied extensively across the PARWM with microglial markers significantly higher in the subventricular region compared to either the middle‐zone (CD68 p = 0.028, IBA1 p < 0.001, MHC‐II p < 0.001) or subcortical region (CD68 p = 0.002, IBA1 p < 0.001, MHC‐II p < 0.001). Clasmatodendritic (CD) GFAP+ astrocytes significantly increased from the subcortical to the subventricular region (p < 0.001), whilst GFAP+ stellate astrocytes significantly decreased (p < 0.001). Cellular reactions could be grouped into two distinct patterns: an immune response associated with MHC‐II/IBA1 expression and CD astrocytes; and a more innate response characterised by CD68 expression associated with WML. White matter neuroinflammation showed weak relationships to the measures of SVD, but not to the measures of AD neuropathology. In conclusion, glial responses vary extensively across the PARWM with diverse patterns of white matter neuroinflammation. Although these findings support a role for vascular factors in the pathogenesis of age‐related white matter neuroinflammation, additional factors other than SVD and AD pathology may drive this. Understanding the heterogeneity in white matter neuroinflammation will be important for the therapeutic targeting of age‐associated white matter damage

    A PDZ-containing Scaffold Related to the Dystrophin Complex at the Basolateral Membrane of Epithelial Cells

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    Membrane scaffolding complexes are key features of many cell types, serving as specialized links between the extracellular matrix and the actin cytoskeleton. An important scaffold in skeletal muscle is the dystrophin-associated protein complex. One of the proteins bound directly to dystrophin is syntrophin, a modular protein comprised entirely of interaction motifs, including PDZ (protein domain named for PSD-95, discs large, ZO-1) and pleckstrin homology (PH) domains. In skeletal muscle, the syntrophin PDZ domain recruits sodium channels and signaling molecules, such as neuronal nitric oxide synthase, to the dystrophin complex. In epithelia, we identified a variation of the dystrophin complex, in which syntrophin, and the dystrophin homologues, utrophin and dystrobrevin, are restricted to the basolateral membrane. We used exogenously expressed green fluorescent protein (GFP)-tagged fusion proteins to determine which domains of syntrophin are responsible for its polarized localization. GFP-tagged full-length syntrophin targeted to the basolateral membrane, but individual domains remained in the cytoplasm. In contrast, the second PH domain tandemly linked to a highly conserved, COOH-terminal region was sufficient for basolateral membrane targeting and association with utrophin. The results suggest an interaction between syntrophin and utrophin that leaves the PDZ domain of syntrophin available to recruit additional proteins to the epithelial basolateral membrane. The assembly of multiprotein signaling complexes at sites of membrane specialization may be a widespread function of dystrophin-related protein complexes

    Genotype and Gene Expression Associations with Immune Function in Drosophila

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    It is now well established that natural populations of Drosophila melanogaster harbor substantial genetic variation associated with physiological measures of immune function. In no case, however, have intermediate measures of immune function, such as transcriptional activity of immune-related genes, been tested as mediators of phenotypic variation in immunity. In this study, we measured bacterial load sustained after infection of D. melanogaster with Serratia marcescens, Providencia rettgeri, Enterococcus faecalis, and Lactococcus lactis in a panel of 94 third-chromosome substitution lines. We also measured transcriptional levels of 329 immune-related genes eight hours after infection with E. faecalis and S. marcescens in lines from the phenotypic tails of the test panel. We genotyped the substitution lines at 137 polymorphic markers distributed across 25 genes in order to test for statistical associations among genotype, bacterial load, and transcriptional dynamics. We find that genetic polymorphisms in the pathogen recognition genes (and particularly in PGRP-LC, GNBP1, and GNBP2) are most significantly associated with variation in bacterial load. We also find that overall transcriptional induction of effector proteins is a significant predictor of bacterial load after infection with E. faecalis, and that a marker upstream of the recognition gene PGRP-SD is statistically associated with variation in both bacterial load and transcriptional induction of effector proteins. These results show that polymorphism in genes near the top of the immune system signaling cascade can have a disproportionate effect on organismal phenotype due to the amplification of minor effects through the cascade

    Arginine Metabolism by Macrophages Promotes Cardiac and Muscle Fibrosis in mdx Muscular Dystrophy

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    Duchenne muscular dystrophy (DMD) is the most common, lethal disease of childhood. One of 3500 new-born males suffers from this universally-lethal disease. Other than the use of corticosteroids, little is available to affect the relentless progress of the disease, leading many families to use dietary supplements in hopes of reducing the progression or severity of muscle wasting. Arginine is commonly used as a dietary supplement and its use has been reported to have beneficial effects following short-term administration to mdx mice, a genetic model of DMD. However, the long-term effects of arginine supplementation are unknown. This lack of knowledge about the long-term effects of increased arginine metabolism is important because elevated arginine metabolism can increase tissue fibrosis, and increased fibrosis of skeletal muscles and the heart is an important and potentially life-threatening feature of DMD.We use both genetic and nutritional manipulations to test whether changes in arginase metabolism promote fibrosis and increase pathology in mdx mice. Our findings show that fibrotic lesions in mdx muscle are enriched with arginase-2-expressing macrophages and that muscle macrophages stimulated with cytokines that activate the M2 phenotype show elevated arginase activity and expression. We generated a line of arginase-2-null mutant mdx mice and found that the mutation reduced fibrosis in muscles of 18-month-old mdx mice, and reduced kyphosis that is attributable to muscle fibrosis. We also observed that dietary supplementation with arginine for 17-months increased mdx muscle fibrosis. In contrast, arginine-2 mutation did not reduce cardiac fibrosis or affect cardiac function assessed by echocardiography, although 17-months of dietary supplementation with arginine increased cardiac fibrosis. Long-term arginine treatments did not decrease matrix metalloproteinase-2 or -9 or increase the expression of utrophin, which have been reported as beneficial effects of short-term treatments.Our findings demonstrate that arginine metabolism by arginase promotes fibrosis of muscle in muscular dystrophy and contributes to kyphosis. Our findings also show that long-term, dietary supplementation with arginine exacerbates fibrosis of dystrophic heart and muscles. Thus, commonly-practiced dietary supplementation with arginine by DMD patients has potential risk for increasing pathology when performed for long periods, despite reports of benefits acquired with short-term supplementation

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∌99% of the euchromatic genome and is accurate to an error rate of ∌1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead
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