245 research outputs found
Working with Immigrant and Refugee Deaf Students: Strategies and Decision-Making Processes of Interpreters
This study investigates the work of educational interpreters working with D/deaf and hard of hearing (DHH) students who are refugees or immigrants. This investigation occurs at the intersection of several fields of study: American Sign Language (ASL) interpreting, Deaf education, and immigrant and refugee education. Despite the overlap in these fields found in interpreters’ work with DHH refugee and immigrant students, to date no research has studied this work. This pilot study, conducted through four interviews of interpreters working in K-12 settings with DHH refugees and immigrants, explores the current practices of these interpreters in these settings. These practices are current practices and are not to be considered best practices. Interviews focus on the strategies interpreters use, as well as the decision-making processes behind these strategies. Results from this study suggest that interpreters use communication with the educational team, frequently outside of interpreting, with the goals of a) problem-solving and collaborating, b) following or making alterations to the IEP, and c) fostering student-teacher relationships. Interpreters also use communication strategies with DHH refugee and immigrant students during and outside of interpreting, including a) modifying the interpreter’s language use, b) taking on additional responsibilities, c) establishing and maintaining relationships with students, d) monitoring student comprehension, e) fostering students’ self-esteem, and f) encouraging communication with parents in order to foster DHH refugee and immigrant students’ linguistic, academic, social, and emotional growth. The interpreters in this study also communicate with DHH refugee and immigrant students’ peers and use interpreting strategies to facilitate interactions with DHH refugee and immigrant students and educators or peers. Interpreters use these strategies to foster the growth and success of DHH refugee and immigrant students in K-12 environments
Exact results for quantum phase transitions in random XY spin chains
The effect of disorder on the quantum phase transitions induced by a
transverse field, anisotropy, and dimerization in XY spin chains is
investigated. The low-energy behavior near the critical point is described by a
Dirac-type equation with a random mass for which an exact analytic treatment is
possible. Results obtained for the dynamical critical exponent, the specific
heat, and transverse susceptibility agree with results recently obtained using
a real space renormalization group decimation technique, supporting Fisher's
claim that it is exact. A non-zero transverse field changes the universality
class of the anisotropy transition.Comment: 5 pages, RevTeX + epsf, 2 figures
Universal subgap optical conductivity in quasi-one-dimensional Peierls systems
Quasi-one-dimensional Peierls systems with quantum and thermal lattice
fluctuations can be modeled by a Dirac-type equation with a Gaussian-correlated
off-diagonal disorder. A powerful new method gives the exact disorder-averaged
Green function used to compute the optical conductivity. The strong subgap tail
of the conductivity has a universal scaling form. The frequency and temperature
dependence of the calculated spectrum agrees with experiments on KCP(Br) and
trans-polyacetylene.Comment: 11 pages (+ 3 figures), LATEX (REVTEX 3.0
Mechanisms, models and biomarkers in amyotrophic lateral sclerosis
The last 30 years have seen a major advance in the understanding of the clinical and pathological heterogeneity of amyotrophic lateral sclerosis (ALS), and its overlap with frontotemporal dementia. Multiple, seemingly disparate biochemical pathways converge on a common clinical syndrome characterized by progressive loss of upper and lower motor neurons. Pathogenic themes in ALS include excitotoxicity, oxidative stress, mitochondrial dysfunction, neuroinflammation, altered energy metabolism, and most recently RNA mis-processing. The transgenic rodent, overexpressing mutant superoxide dismutase-1, is now only one of several models of ALS pathogenesis. The nematode, fruit fly and zebrafish all offer fresh insight, and the development of induced pluripotent stem cell-derived motor neurons holds promise for the screening of candidate therapeutics. The lack of useful biomarkers in ALS contributes to diagnostic delay, and the inability to stratify patients by prognosis may be an important factor in the failure of therapeutic trials. Biomarkers sensitive to disease activity might lessen reliance on clinical measures and survival as trial endpoints and reduce study length. Emerging proteomic markers of neuronal loss and glial activity in cerebrospinal fluid, a cortical signature derived from advanced structural and functional MRI, and the development of more sensitive measurements of lower motor neuron physiology are leading a new phase of biomarker-driven therapeutic discovery
Effect of disorder on quantum phase transitions in anisotropic XY spin chains in a transverse field
We present some exact results for the effect of disorder on the critical
properties of an anisotropic XY spin chain in a transverse field. The continuum
limit of the corresponding fermion model is taken and in various cases results
in a Dirac equation with a random mass. Exact analytic techniques can then be
used to evaluate the density of states and the localization length. In the
presence of disorder the ferromagnetic-paramagnetic or Ising transition of the
model is in the same universality class as the random transverse field Ising
model solved by Fisher using a real space renormalization group decimation
technique (RSRGDT). If there is only randomness in the anisotropy of the
magnetic exchange then the anisotropy transition (from a ferromagnet in the
direction to a ferromagnet in the direction) is also in this universality
class. However, if there is randomness in the isotropic part of the exchange or
in the transverse field then in a non-zero transverse field the anisotropy
transition is destroyed by the disorder. We show that in the Griffiths' phase
near the Ising transition that the ground state energy has an essential
singularity. The results obtained for the dynamical critical exponent, the
typical correlation length, and the temperature dependence of the specific heat
near the Ising transition agree with the results of the RSRGDT and numerical
work.Comment: 22 pages, RevTeX + epsf, 4 figure
Mechanisms Models and Biomarkers in Amyotrophic Lateral Sclerosis
The last 30 years have seen a major advance in the understanding of the clinical and pathological heterogeneity of amyotrophic lateral sclerosis (ALS), and its overlap with frontotemporal dementia. Multiple, seemingly disparate biochemical pathways converge on a common clinical syndrome characterized by progressive loss of upper and lower motor neurons. Pathogenic themes in ALS include excitotoxicity, oxidative stress, mitochondrial dysfunction, neuroinflammation, altered energy metabolism, and most recently RNA mis-processing. The transgenic rodent, overexpressing mutant superoxide dismutase-1, is now only one of several models of ALS pathogenesis. The nematode, fruit fly and zebrafish all offer fresh insight, and the development of induced pluripotent stem cell-derived motor neurons holds promise for the screening of candidate therapeutics. The lack of useful biomarkers in ALS contributes to diagnostic delay, and the inability to stratify patients by prognosis may be an important factor in the failure of therapeutic trials. Biomarkers sensitive to disease activity might lessen reliance on clinical measures and survival as trial endpoints and reduce study length. Emerging proteomic markers of neuronal loss and glial activity in cerebrospinal fluid, a cortical signature derived from advanced structural and functional MRI, and the development of more sensitive measurements of lower motor neuron physiology are leading a new phase of biomarker-driven therapeutic discovery
Early onset and novel features in a spinal and bulbar muscular atrophy patient with a 68 CAG repeat
AbstractSpinal and bulbar muscular atrophy (SBMA) is an X-linked neuromuscular disease caused by a trinucleotide (CAG) repeat expansion in the androgen receptor gene. Patients with SBMA have weakness, atrophy, and fasciculations in the bulbar and extremity muscles. Individuals with CAG repeat lengths greater than 62 have not previously been reported. We evaluated a 29year old SBMA patient with 68 CAGs who had unusually early onset and findings not seen in others with the disease. Analysis of the androgen receptor gene confirmed the repeat length of 68 CAGs in both peripheral blood and fibroblasts. Evaluation of muscle and sensory function showed deficits typical of SBMA, and in addition the patient had manifestations of autonomic dysfunction and abnormal sexual development. These findings extend the known phenotype associated with SBMA and shed new insight into the effects of the mutated androgen receptor
A randomized controlled trial of exercise in spinal and bulbar muscular atrophy.
OBJECTIVE: To determine the safety and efficacy of a home-based functional exercise program in spinal and bulbar muscular atrophy (SBMA).
METHODS: Subjects were randomly assigned to participate in 12 weeks of either functional exercises (intervention) or a stretching program (control) at the National Institutes of Health in Bethesda, MD. A total of 54 subjects enrolled, and 50 completed the study with 24 in the functional exercise group and 26 in the stretching control group. The primary outcome measure was the Adult Myopathy Assessment Tool (AMAT) total score, and secondary measures included total activity by accelerometry, muscle strength, balance, timed up and go, sit-to-stand test, health-related quality of life, creatine kinase, and insulin-like growth factor-1.
RESULTS: Functional exercise was well tolerated but did not lead to significant group differences in the primary outcome measure or any of the secondary measures. The functional exercise did not produce significantly more adverse events than stretching, and was not perceived to be difficult. To determine whether a subset of the subjects may have benefited, we divided them into high and low functioning based on baseline AMAT scores and performed a post hoc subgroup analysis. Low-functioning individuals receiving the intervention increased AMAT functional subscale scores compared to the control group.
INTERPRETATION: Although these trial results indicate that functional exercise had no significant effect on total AMAT scores or on mobility, strength, balance, and quality of life, post hoc findings indicate that low-functioning men with SBMA may respond better to functional exercises, and this warrants further investigation with appropriate exercise intensity
A motor neuron disease–associated mutation in p150Glued perturbs dynactin function and induces protein aggregation
The microtubule motor cytoplasmic dynein and its activator dynactin drive vesicular transport and mitotic spindle organization. Dynactin is ubiquitously expressed in eukaryotes, but a G59S mutation in the p150Glued subunit of dynactin results in the specific degeneration of motor neurons. This mutation in the conserved cytoskeleton-associated protein, glycine-rich (CAP-Gly) domain lowers the affinity of p150Glued for microtubules and EB1. Cell lines from patients are morphologically normal but show delayed recovery after nocodazole treatment, consistent with a subtle disruption of dynein/dynactin function. The G59S mutation disrupts the folding of the CAP-Gly domain, resulting in aggregation of the p150Glued protein both in vitro and in vivo, which is accompanied by an increase in cell death in a motor neuron cell line. Overexpression of the chaperone Hsp70 inhibits aggregate formation and prevents cell death. These data support a model in which a point mutation in p150Glued causes both loss of dynein/dynactin function and gain of toxic function, which together lead to motor neuron cell death
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