The Greatest Evasion: Why Technology Won\u27t Save Education

Americans place an enormous amount of faith in education=s power to solve social problems. Today, liberals tend to believe that education can improve our attitudes, making us less racist by broadening our perspective and knowledge of different people and cultures. Conservatives often argue that education can solve our economic problems by training citizens for jobs and increasing their capacity for upward social mobility. Indeed, President Clinton, who may be viewed as bridging liberal and conservative ideals, posed education as a solution to economic dislocation. His solution is to provide unemployed citizens with the necessary skills to find new forms of employment. Education, it would seem, stands as a primary pillar of American democracy

The Greatest Evasion: Why Technology Won\u27t Save Education

Americans place an enormous amount of faith in education=s power to solve social problems. Today, liberals tend to believe that education can improve our attitudes, making us less racist by broadening our perspective and knowledge of different people and cultures. Conservatives often argue that education can solve our economic problems by training citizens for jobs and increasing their capacity for upward social mobility. Indeed, President Clinton, who may be viewed as bridging liberal and conservative ideals, posed education as a solution to economic dislocation. His solution is to provide unemployed citizens with the necessary skills to find new forms of employment. Education, it would seem, stands as a primary pillar of American democracy

Swarm Mechanics and Swarm Chemistry: A Transdisciplinary Approach for Robot Swarms

This paper for the first time attempts to bridge the knowledge between chemistry, fluid mechanics, and robot swarms. By forming these connections, we attempt to leverage established methodologies and tools from these these domains to uncover how we can better comprehend swarms. The focus of this paper is in presenting a new framework and sharing the reasons we find it promising and exciting. While the exact methods are still under development, we believe simply laying out a potential path towards solutions that have evaded our traditional methods using a novel method is worth considering. Our results are characterized through both simulations and real experiments on ground robots.Comment: 7 pages, 11 figures, submitted to ICRA 2024 conferenc

Nontelomeric TRF2-REST Interaction Modulates Neuronal Gene Silencing and Fate of Tumor and Stem Cells

SummaryRemoval of TRF2, a telomere shelterin protein, recapitulates key aspects of telomere attrition including the DNA-damage response and cell-cycle arrest [1]. Distinct from the response of proliferating cells to loss of TRF2 [2, 3], in rodent noncycling cells, TRF2 inhibition promotes differentiation and growth [4, 5]. However, the mechanism that couples telomere gene-silencing features [6–8] to differentiation programs has yet to be elucidated. Here we describe an extratelomeric function of TRF2 in the regulation of neuronal genes mediated by the interaction of TRF2 with repressor element 1-silencing transcription factor (REST), a master repressor of gene networks devoted to neuronal functions [9–12]. TRF2-REST complexes are readily detected by coimmunoprecipitation assays and are localized to aggregated PML-nuclear bodies in undifferentiated pluripotent human NTera2 stem cells. Inhibition of TRF2, either by a dominant-negative mutant or by RNA interference, dissociates TRF2-REST complexes resulting in ubiquitin-proteasomal degradation of REST. Consequentially, REST-targeted neural genes (L1CAM, β3-tubulin, synaptophysin, and others) are derepressed, resulting in acquisition of neuronal phenotypes. Notably, selective damage to telomeres without affecting TRF2 levels causes neither REST degradation nor cell differentiation. Thus, in addition to protecting telomeres, TRF2 possesses a novel role in stabilization of REST thereby controlling neural tumor and stem cell fate

Edusource: Canada's Learning Object Repository Network

An alliance of Canadian Universities and government agencies pooled their resources to establish a network to share and combine Learning Objects from a variety of sources and further develop this technology. In the process, they resolved many learning, logistical, and legal problems and moved this technology forward by an order of magnitude. Principal goals include: nationwide interoperability, network of repositories, linked servers, repository software programs, national and international standards, digital rights management, business and management models, evaluation and feedback, dissemination of results, and bilingual access to all Canadians, particularly learners with disabilities. The defined tasks were sub-divided into nine work packages, each with a lead institution as package manager

Conserved and Differential Effects of Dietary Energy Intake on the Hippocampal Transcriptomes of Females and Males

The level of dietary energy intake influences metabolism, reproductive function, the development of age-related diseases, and even cognitive behavior. Because males and females typically play different roles in the acquisition and allocation of energy resources, we reasoned that dietary energy intake might differentially affect the brains of males and females at the molecular level. To test this hypothesis, we performed a gene array analysis of the hippocampus in male and female rats that had been maintained for 6 months on either ad libitum (control), 20% caloric restriction (CR), 40% CR, intermittent fasting (IF) or high fat/high glucose (HFG) diets. These diets resulted in expected changes in body weight, and circulating levels of glucose, insulin and leptin. However, the CR diets significantly increased the size of the hippocampus of females, but not males. Multiple genes were regulated coherently in response to energy restriction diets in females, but not in males. Functional physiological pathway analyses showed that the 20% CR diet down-regulated genes involved in glycolysis and mitochondrial ATP production in males, whereas these metabolic pathways were up-regulated in females. The 40% CR diet up-regulated genes involved in glycolysis, protein deacetylation, PGC-1α and mTor pathways in both sexes. IF down-regulated many genes in males including those involved in protein degradation and apoptosis, but up-regulated many genes in females including those involved in cellular energy metabolism, cell cycle regulation and protein deacetylation. Genes involved in energy metabolism, oxidative stress responses and cell death were affected by the HFG diet in both males and females. The gender-specific molecular genetic responses of hippocampal cells to variations in dietary energy intake identified in this study may mediate differential behavioral responses of males and females to differences in energy availability

Gene expression atlas of the mouse central nervous system: impact and interactions of age, energy intake and gender

The transcriptional profiles of five regions of the central nervous system (CNS) of mice varying in age, gender and dietary intake were measured by microarray. The resulting data provide insights into the mechanisms of age-, diet- and gender-related CNS plasticity and vulnerability in mammals

Differential levels of glutamate dehydrogenase 1 (GLUD1) in Balb/c and C57BL/6 mice and the effects of overexpression of the Glud1 gene on glutamate release in striatum

We have previously shown that overexpression of the Glud1 (glutamate dehydrogenase 1) gene in neurons of C57BL/6 mice results in increased depolarization-induced glutamate release that eventually leads to selective neuronal injury and cell loss by 12 months of age. However, it is known that isogenic lines of Tg (transgenic) mice produced through back-crossing with one strain may differ in their phenotypic characteristics from those produced using another inbred mouse strain. Therefore, we decided to introduce the Glud1 transgene into the Balb/c strain that has endogenously lower levels of GLUD1 (glutamate dehydrogenase 1) enzyme activity in the brain as compared with C57BL/6. Using an enzyme-based MEA (microelectrode array) that is selective for measuring glutamate in vivo, we measured depolarization-induced glutamate release. Within a discrete layer of the striatum, glutamate release was significantly increased in Balb/c Tg mice compared with wt (wild-type) littermates. Furthermore, Balb/c mice released approx. 50–60% of the amount of glutamate compared with C57BL/6 mice. This is similar to the lower levels of endogenous GLUD1 protein in Balb/c compared with C57BL/6 mice. The development of these Glud1-overexpressing mice may allow for the exploration of key molecular events produced by chronic exposure of neurons to moderate, transient increases in glutamate release, a process hypothesized to occur in neurodegenerative disorders

Transcriptional changes in the rat brain induced by repetitive transcranial magnetic stimulation

IntroductionTranscranial Magnetic Stimulation (TMS) is a noninvasive technique that uses pulsed magnetic fields to affect the physiology of the brain and central nervous system. Repetitive TMS (rTMS) has been used to study and treat several neurological conditions, but its complex molecular basis is largely unexplored.MethodsUtilizing three experimental rat models (in vitro, ex vivo, and in vivo) and employing genome-wide microarray analysis, our study reveals the extensive impact of rTMS treatment on gene expression patterns.ResultsThese effects are observed across various stimulation protocols, in diverse tissues, and are influenced by time and age. Notably, rTMS-induced alterations in gene expression span a wide range of biological pathways, such as glutamatergic, GABAergic, and anti-inflammatory pathways, ion channels, myelination, mitochondrial energetics, multiple neuron-and synapse-specific genes.DiscussionThis comprehensive transcriptional analysis induced by rTMS stimulation serves as a foundational characterization for subsequent experimental investigations and the exploration of potential clinical applications