Holo-Stroke: Assessing for Immersive Stroke Care Through Stroke Hologram Teleportation.

Background: Augmented reality enables the wearer to see both their physical environment and virtual objects. Holograms could allow 3D video of providers to be transmitted to distant sites, allowing patients to interact with virtual providers as if they are in the same physical space. Our aim was to determine if Tele-Stroke augmented with Holo-Stroke, compared with Tele-Stroke alone, could improve satisfaction and perception of immersion for the patient. Methods: Kinect cameras positioned at 90-degree intervals around the hub practitioner were used. Cameras streamed real-time optical video to a unity point-cloud program where the data were stitched together in a 360-degree view. The resultant hologram was positioned in 3D space and was visible through the head-mounted display by the patient. Radiology images were shared in Tele-Stroke and via hologram. Likert satisfaction questions were administered. Wilcoxon signed-rank testing was used. Results: Each of the 30 neurology clinic participants scored both Tele-Stroke and Holo-Stroke. Out of these, 29 patients completed the assessments (1 failure owing to computer reboot). Average age was 52 years, with 53.3% of the patients being female, 70.0% being White, and 13.3% being Hispanic. Likert scale score median "Overall" was 32 Tele-Stroke versus 48 Holo-Stroke (p < 0.00001), "Immersion" was 5 versus 10 (p < 0.00001), "Beneficial Technique" was 6 versus 10 (p < 0.00001), and "Ability to See Images" was 5 versus 10 (p < 0.00001). Discussion: Holo-Stroke 3D holographic Tele-Stroke exams resulted in feasibility, satisfaction, and high perception of immersion for the patient. Patients were enthusiastic for the more immersive, personal discussion with their provider and a robust way to experience radiology images. Though further assessments are needed, Holo-Stroke can help the provider "be there, not just see there!"

The Competitive Effects of School Choice on Student Achievement: A Systematic Review.

School-choice policies are expected to generate healthy competition between schools, leading to improvements in school quality and better outcomes for students. However, the empirical literature testing this assumption yields mixed findings. This systematic review and meta-analysis tests this theory by synthesizing the empirical literature on the competitive effects of school choice on student achievement. Overall, we found small positive effects of competition on student achievement. We also found some evidence that the type of school-choice policy and student demographics moderated the effects of competition on student achievement. By examining whether school competition improves outcomes, our findings can inform decisions of state and local policymakers who have adopted or are considering adopting school-choice reforms.

It's Who You Know: The Role of Social Networks in a Changing Labor Market.

Teacher labor markets are evolving across the United States. The rise of charter schools, alternative teacher certification, and portfolio districts are transforming teachers' access to employment, changing the way they search for and apply for jobs, and may also change the role that social networks play in the job search. However, we know little about how teachers use their networks to find jobs, particularly in increasingly fragmented local labor markets. We draw on interviews with 127 teachers in three districts chosen to reflect an increasing presence of charter schools: New Orleans, Detroit, and San Antonio. We find that the extent of fragmentation in a city's labor market drives the use of networks, with important implications for job access and equity.

To Switch or Not to Switch? The Influence of School Choice and Labor Market Segmentation on Teachers' Job Searches.

Informal and institutional barriers may limit teacher movement between charter schools and traditional public schools (TPSs). However, we know little about how teachers choose schools in areas with a robust charter school sector. This study uses qualitative data from 123 teachers to examine teachers' job decisions in three cities with varying charter densities: San Antonio, Detroit, and New Orleans. Our findings illuminate different types of segmentation and factors that facilitate and limit mobility between sectors. We find that structural policies within each sector can create barriers to mobility across charter schools and TPSs and that teachers' ideological beliefs and values serve as informal, personal barriers that reinforce divides between sectors. This study offers implications for policy in districts with school choice.

Gender, Markets, and Inequality: A Framework.

A growing body of research examines the role of elite networks, power, and race in the advocacy for market-based reforms and their ultimate effects on students, teachers, and communities of color. Yet, less research explores how such reforms interact with gender in the workplace, especially how policies such as school choice, competition, and incentive-based pay impact female actors within K-12 schools (e.g., teachers, school leaders). The current research on marketization and privatization in education has largely overlooked the potential impact on women in schools. We review the literature on women in K-12 education and in the economy more generally, and organize it conceptually to identify areas for future inquiry. After synthesizing and summarizing themes across diverse bodies of literature, we contend that as schools privatize, we may see greater gender disparities in education leadership and teaching.

Role of ß4 integrin phosphorylation in human invasive squamous cell carcinoma: regulation of hemidesmosome stability modulates cell migration.

Hemidesmosomes (HDs) are multiprotein structures that anchor epithelia to the basement membrane. During squamous cell carcinoma (SCC) invasion, there is a reduction in the number of HDs, which may facilitate dissemination. Mechanisms of HD disassembly are incompletely understood. Previous work has shown that epidermal growth factor (EGF)-induced phosphorylation of the ß4 integrin on three of its serines, S(1356)S(1360)S(1364), can induce HD disassembly in normal cells. Here, we examine the role of ß4 integrin serine phosphorylation in SCC. We have found that around 60% of invasive cutaneous SCC show increased ß4 phosphorylation on S(1356) when compared with carcinoma in situ or normal tissue. To assess the mechanisms by which SCC increases ß4 phosphorylation, we performed in vitro analyses. Compared with keratinocytes, SCC cells showed increased levels of S(1356) phosphorylation in the absence of EGF, correlating with reduced HD-like structures. In addition, phospho-S(1356) signal was largely segregated from other HD components. Epidermal growth factor receptor and PKC inhibitors inhibited basal levels of S(1356) phosphorylation in SCC, suggesting that cells use intrinsic mechanisms to activate the EGF signaling pathway to induce ß4 phosphorylation. Moreover, these inhibitors stabilized HD-like structures in SCC cells and reduced their migratory ability. Mutation of S(1356)S(1360)S(1364) in SCC cells to non-phosphorylatable alanines stabilized HD-like structures and substantially reduced migration, while mutation into phosphorylation mimicking aspartate reduced HD-like structures but had no effect on migration, suggesting that serine phosphorylation function is releasing anchorage rather than promoting migration. Altogether these results suggest that ß4 serine phosphorylation may have an important role during SCC invasion by destabilizing HDs and facilitating migration.

Rethinking Teacher Turnover: Longitudinal Measures of Instability in Schools.

While there is a robust literature examining the patterns and causes of teacher turnover, few articles to date have critically examined the measures of turnover used in these studies. Yet, an assessment of the way turnover is measured is important, as the measures become the means by which the "problem" of turnover becomes defined and its varying dimensions understood. In this conceptual essay, we outline a typology of teacher turnover measures, discussing both measures used in existing teacher turnover literature as well as new measures that we have developed. We illustrate each of the measures using 10 years of administrative data from Texas. We discuss how the measures can help illuminate different ways in which staff instability can affect schools and identify schools that suffer from particularly severe staffing issues. We conclude with implications for policymakers and researchers who may seek to apply these measures to future empirical studies.

Thyroid hormone homeostasis and action in the type 2 deiodinase-deficient rodent brain during development.

Considerable indirect evidence suggests that the type 2 deiodinase (D2) generates T3 from T4 for local use in specific tissues such as pituitary, brown fat, and brain, and studies with a D2-deficent mouse, the D2 knockout (D2KO) mouse, have shown this to be the case in pituitary and brown fat. The present study employs the D2KO mouse to determine the role of D2 in the developing brain. As expected, the T3 content in the neonatal D2KO brain was markedly reduced to a level comparable with that seen in the hypothyroid neonatal wild-type mouse. However, the mRNA levels of several T3-responsive genes were either unaffected or much less affected in the brain of the D2KO mouse than in that of the hypothyroid mouse, and compared with the hypothyroid mouse, the D2KO mouse exhibited a very mild neurological phenotype. The current view of thyroid hormone homeostasis in the brain dictates that the T3 present in neurons is generated mostly, if not exclusively, from T4 by the D2 in glial cells. This view is inadequate to explain the findings presented herein, and it is suggested that important compensatory mechanisms must be in play in the brain to minimize functional abnormalities in the absence of the D2.

Targeted disruption of the type 1 selenodeiodinase gene (Dio1) results in marked changes in thyroid hormone economy in mice.

The type 1 deiodinase (D1) is thought to be an important source of T3 in the euthyroid state. To explore the role of the D1 in thyroid hormone economy, a D1-deficient mouse (D1KO) was made by targeted disruption of the Dio1 gene. The general health and reproductive capacity of the D1KO mouse were seemingly unimpaired. In serum, levels of T4 and rT3 were elevated, whereas those of TSH and T3 were unchanged, as were several indices of peripheral thyroid status. It thus appears that the D1 is not essential for the maintenance of a normal serum T3 level in euthyroid mice. However, D1 deficiency resulted in marked changes in the metabolism and excretion of iodothyronines. Fecal excretion of endogenous iodothyronines was greatly increased. Furthermore, when compared with both wild-type and D2-deficient mice, fecal excretion of [125I]iodothyronines was greatly increased in D1KO mice during the 48 h after injection of [125I]T4 or [125I]T3, whereas urinary excretion of [125I]iodide was markedly diminished. From these data it was estimated that a majority of the iodide generated by the D1 was derived from substrates other than T4. Treatment with T3 resulted in a significantly higher serum T3 level and a greater degree of hyperthyroidism in D1KO mice than in wild-type mice. We conclude that, although the D1 is of questionable importance to the wellbeing of the euthyroid mouse, it may play a major role in limiting the detrimental effects of conditions that alter normal thyroid function, including hyperthyroidism and iodine deficiency.

Determinants of iodothyronine deiodinase activities in rodent uterus.

The deiodinase types 2 and 3 (D2, D3), which convert T4 to active and inactive metabolites, respectively, are expressed in the rodent uterus and highly induced during pregnancy. To examine the factors regulating the expression of these enzymes in this tissue, we studied D2 and D3 activity in pregnant rats, in pseudopregnant rats before and after the induction of artificial decidualization, and in ovariectomized rats treated with 17beta-estradiol (E2) and/or progesterone (P). Our results demonstrate that induction of D3 activity begins immediately after implantation and increases markedly over the next 72 h. A similar time course and magnitude of D3 induction is noted in the artificially decidualized uterus in pseudopregnant rats, whereas only minimal increases in activity are observed in the nondecidualized control uterine horns in the same animal. In contrast, D2 activity is not induced by a decidualization stimulus. In spontaneously cycling female rats, both D2 and D3 were observed to be 3- to 8-fold higher in proestrus, compared with diestrus. Furthermore, levels of D2 and D3 activity were greatly increased in ovariectomized rats given E2 and P in various combinations. D2 activity was stimulated primarily by E2, whereas E2 and P acted synergistically to increase D3 activity. These results demonstrate that E2 and P regulate thyroid hormone metabolism in the uterus, and that the implantation process is a potent stimulus for the induction of D3 activity in this organ. Such precise and profound changes in deiodinase expression are likely to play important physiological roles in fetal development and may influence uterine function.

Phosphorylation of a novel site on the {beta}4 integrin at the trailing edge of migrating cells promotes hemidesmosome disassembly.

Hemidesmosomes (HDs) are multiprotein structures that anchor epithelial cells to the basement membrane. HD components include the alpha6beta4 integrin, plectin, and BPAGs (bullous pemphigoid antigens). HD disassembly in keratinocytes is necessary for cells to migrate and can be induced by EGF through beta4 integrin phosphorylation. We have identified a novel phosphorylation site on the beta4 integrin: S(1424). Preventing phosphorylation by mutating S-->A(1424) results in increased incorporation of beta4 into HDs and resistance to EGF-induced disassembly. In contrast, mutating S-->D(1424) (mimicking phosphorylation) partially mobilizes beta4 from HDs and potentiates the disassembly effects of other phosphorylation sites. In contrast to previously described sites that are phosphorylated upon growth factor stimulation, S(1424) already exhibits high constitutive phosphorylation, suggesting additional functions. Constitutive phosphorylation of S(1424) is distinctively enriched at the trailing edge of migrating keratinocytes where HDs are disassembled. Although most of this S(1424)-phosphorylated beta4 is found dissociated from HDs, a substantial amount can be associated with HDs near the cell margins, colocalizing with plectin but always excluding BPAGs, suggesting that phospho-S(1424) might be a mechanism to dissociate beta4 from BPAGs. S(1424) phosphorylation is PKC dependent. These data suggest an important role for S(1424) in the gradual disassembly of HDs induced by cell retraction.