126 research outputs found
Interactive Water Vortex Exhibit
The San Luis Obispo Children’s Museum requested an interactive water vortex exhibit to both engage and entertain inquisitive guests, ages two to eight. The goal was to design and manufacture an exhibit that would educate its users on the fluid mechanics behind water vortices. They activate the mechanics by spinning a wheel, which is perceived as the catalyst to manipulate the flow of water to successfully create a whirlpool. Our team has created an interactive display that will enlighten young minds, providing the museum with an educational exhibit which shares a concept not currently taught by any other. Our project takes the manual input, as provided by a child, and translates it to a digital signal that can be read by a motor, to spin a magnet, that creates enough speed to spiral the water. The final prototype was manufactured and tested to allow children to provide minimal input to produce a water vortex
Levels in the toposes of simplicial sets and cubical sets
The essential subtoposes of a fixed topos form a complete lattice, which
gives rise to the notion of a level in a topos. In the familiar example of
simplicial sets, levels coincide with dimensions and give rise to the usual
notions of n-skeletal and n-coskeletal simplicial sets. In addition to the
obvious ordering, the levels provide a stricter means of comparing the
complexity of objects, which is determined by the answer to the following
question posed by Bill Lawvere: when does n-skeletal imply k-coskeletal? This
paper answers this question for several toposes of interest to homotopy theory
and higher category theory: simplicial sets, cubical sets, and reflexive
globular sets. For the latter, n-skeletal implies (n+1)-coskeletal but for the
other two examples the situation is considerably more complicated: n-skeletal
implies (2n-1)-coskeletal for simplicial sets and 2n-coskeletal for cubical
sets, but nothing stronger. In a discussion of further applications, we prove
that n-skeletal cyclic sets are necessarily (2n+1)-coskeletal.Comment: This paper subsumes earlier work of the first, third, and fourth
authors. 19 page
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High thymidylate synthase gene expression predicts poor outcome after resection of hepatocellular carcinoma.
IntroductionPrognosis after resection of hepatocellular carcinoma (HCC) is highly variable. Compared to clinicopathologic factors, the use of molecular markers to predict outcome has not been well studied. We investigated the prognostic importance of thymidylate synthase (TS) gene expression and polymorphisms in patients after resection of HCC.MethodsPatients who underwent complete resection of HCC for whom tissue was available were identified. TS gene expression level and polymorphisms were determined in HCC specimens. Prognostic factors were evaluated using Kaplan-Meier curves and Cox proportional hazard models.ResultsThe study included 67 patients. In univariate analysis, variables that negatively influenced survival included TNM stage, microvascular invasion, and high TS expression. For the high TS expression group, median survival was 54 months and 5-year actuarial survival was 47%. For the low TS expression group, median survival was not reached and the 5-year actuarial survival was 91%. In multivariate analysis, only high TS expression remained an independent predictor of poor survival (HR = 10.77, 95% CI 1.36-84.91; P = 0.02). TS gene polymorphisms were not associated with TS expression or overall survival.ConclusionsHigh TS expression predicts poor outcome after resection of HCC. Molecular markers might be robust predictors of patient outcome after resection of HCC
Speaking of Online Learning: Alternative Practice-Based Learning Experiences for Speech Pathologists in Australia, Ghana and Hong Kong
Speech Pathology programs usually send students to workplaces to learn clinical skills necessary for practice. During COVID-19, programs needed to respond quickly to ensure that students continued to gain the necessary experiences and skills required to progress through their program and graduate as clinicians, while simultaneously complying with COVID-19 requirements. Case studies from seven different universities in Australia, Ghana and Hong Kong described the diverse ways in which placements were adapted to be COVID-safe, taking into account local needs. Some practices which had been included in placement education prior to the pandemic, such as telepractice and simulation-based learning, were extended and developed during this time. Educators, students, clinicians and clients responded to the rapidly changing needs of the time with flexibility and innovation, utilising a variety of technologies and tools to support case-based and virtual learning opportunities. Feedback from these diverse stakeholders about the experiences was positive, despite inevitable limitations and less-than-ideal circumstances. The positive findings provided insights for consideration in the future: could strategies implemented in response to the pandemic continue to be incorporated into placement experiences, enhancing current practices and maintaining student performance outcomes? Exceptional circumstances prompted exceptional responses; flexibility and innovation were accelerated in response to the pandemic and may transform future placement-based learning opportunities
The role of AmeloD in tooth development
The development of ectodermal organs, such as teeth, requires epithelial–mesenchymal interactions. Basic helix–loop–helix (bHLH) transcription factors regulate various aspects of tissue development, and we have previously identified a bHLH transcription factor, AmeloD, from a tooth germ cDNA library. Here, we provide both in vitro and in vivo evidence that AmeloD is important in tooth development. We created AmeloD-knockout (KO) mice to identify the in vivo functions of AmeloD that are critical for tooth morphogenesis. We found that AmeloD-KO mice developed enamel hypoplasia and small teeth because of increased expression of E-cadherin in inner enamel epithelial (IEE) cells, and it may cause inhibition of the cell migration. We used the CLDE dental epithelial cell line to conduct further mechanistic analyses to determine whether AmeloD overexpression in CLDE cells suppresses E-cadherin expression and promotes cell migration. Knockout of epiprofin (Epfn), another transcription factor required for tooth morphogenesis and development, and analysis of AmeloD expression and deletion revealed that AmeloD also contributed to multiple tooth formation in Epfn-KO mice by promoting the invasion of dental epithelial cells into the mesenchymal region. Thus, AmeloD appears to play an important role in tooth morphogenesis by modulating E-cadherin and dental epithelial–mesenchymal interactions. These findings provide detailed insights into the mechanism of ectodermal organ development
Cellular metabolism constrains innate immune responses in early human ontogeny
Pathogen immune responses are profoundly attenuated in fetuses and premature infants, yet the mechanisms underlying this developmental immaturity remain unclear. Here we show transcriptomic, metabolic and polysome profiling and find that monocytes isolated from infants born early in gestation display perturbations in PPAR-γ-regulated metabolic pathways, limited glycolytic capacity and reduced ribosomal activity. These metabolic changes are linked to a lack of translation of most cytokines and of MALT1 signalosome genes essential to respond to the neonatal pathogen Candida. In contrast, they have little impact on house-keeping phagocytosis functions. Transcriptome analyses further indicate a role for mTOR and its putative negative regulator DNA Damage Inducible Transcript 4-Like in regulating these metabolic constraints. Our results provide a molecular basis for the broad susceptibility to multiple pathogens in these infants, and suggest that the fetal immune system is metabolically programmed to avoid energetically costly, dispensable and potentially harmful immune responses during ontogeny
New Particle-Induced Single Event Latchup Mechanism Observed in a Cryogenic CMOS Readout Integrated Circuit
No abstract availabl
Oncogenic ERBB3 Mutations in Human Cancers
SummaryThe human epidermal growth factor receptor (HER) family of tyrosine kinases is deregulated in multiple cancers either through amplification, overexpression, or mutation. ERBB3/HER3, the only member with an impaired kinase domain, although amplified or overexpressed in some cancers, has not been reported to carry oncogenic mutations. Here, we report the identification of ERBB3 somatic mutations in ∼11% of colon and gastric cancers. We found that the ERBB3 mutants transformed colonic and breast epithelial cells in a ligand-independent manner. However, the mutant ERBB3 oncogenic activity was dependent on kinase-active ERBB2. Furthermore, we found that anti-ERBB antibodies and small molecule inhibitors effectively blocked mutant ERBB3-mediated oncogenic signaling and disease progression in vivo
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