The Balanced Scorecard at Futura Industries

Most companies use the balanced scorecard (BSC) to focus on the financial aspects or the operational metrics required by ISO quality certification. But that is not all one unique company uses the BSC for. At Futura Industries, President Susan Johnson built the enterprise\u27s success over the past 3 years on the BSC\u27s foundational level - the learning, innovation, and growth dimension. This dimension provides the building blocks that generate success in the remaining 3 quadrants: customer service, financial, and internal operations. And the results have followed: a 50% increase in revenue without adding personnel from 1996 to 1999. This organization is all about putting people first. So much so that the company of 300 ranks in the top 10 Family Friendly Employers in Utah for the third year in a row. A look at how they have implemented the 4 quadrants of the BSC using the learning innovation, and growth dimension as their foundation is presented

Teaching as a system: COVID-19 as a lens into teacher change

In the spring of 2020, schools and universities around the world were closed because of the COVID-19 pandemic. The relative lockdown affected more than 1.5 billion learners as teachers and students sheltered at home for several weeks. As schooling moved online, teachers were forced to change how they taught. In the research presented here, we focus on university mathematics professors, and we analyze how their practice, knowledge, and beliefs intertwine and change under these circumstances. More specifically, the context of the pandemic and the relative lockdown provides us with the experimental basis to argue that the new practice affected both knowledge and beliefs of mathematics teachers and that practice, knowledge, and beliefs form a system. Being part of a system, the reactions to change in practice can be of two types, namely, the system as a whole tries to resist change, or the system as a whole changes - and it changes significantly. The research presented here proposes a model for describing and analyzing what we called a teaching system and examines three cases that help to better depict the systemic nature of teaching

Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

Down-regulation of Cdc6, a cell cycle regulatory gene, in prostate cancer

CDC6 plays a critical role in regulation of the onset of DNA replication in eukaryotic cells. We have found that Cdc6 expression is down-regulated in prostate cancer as detected by semiquantitative reverse transcriptase-PCR of prostate cell lines and laser-captured microdissected prostate tissues. This result was substantiated by immunohistochemical analysis of paraffin-embedded tissue sections and immunoblot analysis of benign (BPH-1) and adenocarcinomatous prostatic cells. Furthermore, a 100-fold reduction in the transcription efficiency of the Cdc6 promoter-luciferase construct was noted in the metastatic PC3 cells compared with that in BPH-1 cells. Concentration of the E2F and Oct1 transcription factors that have putative binding sites in the Cdc6 promoter was substantially low in PC3 cells compared with BPH cells. Mutagenesis of the two E2F binding sites on the Cdc6 promoter resulted in increased promoter activity in PC3 cells owing to elimination of the negative regulation by pRb-E2F complex but not to the level of that obtained in BPH cells. We conclude that an altered interaction of transcription factors may be responsible for the down-regulation of Cdc6 transcription in PC3 cells. Our study suggests a potential use of the lack of CDC6 expression as an index of prostate cancer development

Research in Brief - Higher Education in an Era of Mass Incarceration: Possibility Under Constraint

In this essay, we explore the purposes of higher education in prison during an era of mass incarceration and contend that the potential of postsecondary educational opportunity in carceral spaces is undermined by a single-minded focus on reducing recidivism. Among the over 2.2 million individuals behind bars in the United States, only 6 percent have access to formal postsecondary educational opportunities, and as a result, most incarcerated students are not on an educational pathway likely to result in academic degree attainment. We must move beyond a recidivist paradigm not because certificate-based and vocational training is not valuable, but because it is simply not enough of what college-in-prison programming can be or do. Drawing upon the experiences of higher education students who are incarcerated, our analysis reveals how even well-intended practices in prison spaces pose obstacles to seeing incarcerated individuals as potential postsecondary students and degree completers

Cosmic web of galaxies in the COSMOS field:public catalog and different quenching for centrals and satellites

We use a mass complete (log($M/M_{\odot}$) $\geqslant$ 9.6) sample of galaxies with accurate photometric redshifts in the COSMOS field to construct the density field and the cosmic web to $z$=1.2. The comic web extraction relies on the density field Hessian matrix and breaks the density field into clusters, filaments and the field. We provide the density field and cosmic web measures to the community. We show that at $z$ $\lesssim$ 0.8, the median star-formation rate (SFR) in the cosmic web gradually declines from the field to clusters and this decline is especially sharp for satellites ($\sim$ 1 dex vs. $\sim$ 0.5 dex for centrals). However, at $z$ $\gtrsim$ 0.8, the trend flattens out for the overall galaxy population and satellites. For star-forming galaxies only, the median SFR is constant at $z$ $\gtrsim$ 0.5 but declines by $\sim$ 0.3-0.4 dex from the field to clusters for satellites and centrals at $z$ $\lesssim$ 0.5. We argue that for satellites, the main role of the cosmic web environment is to control their star-forming fraction, whereas for centrals, it is mainly to control their overall SFR at $z$ $\lesssim$ 0.5 and to set their fraction at $z$ $\gtrsim$ 0.5. We suggest that most satellites experience a rapid quenching mechanism as they fall from the field into clusters through filaments, whereas centrals mostly undergo a slow environmental quenching at $z$ $\lesssim$ 0.5 and a fast mechanism at higher redshifts. Our preliminary results highlight the importance of the large-scale cosmic web on galaxy evolution

Toward a Manifold Encoding Neural Responses

Understanding circuit properties from physiological data presents two challenges: (i) recordings do not reveal connectivity, and (ii) stimuli only exercise circuits to a limited extent. We address these challenges for the mouse visual system with a novel neural manifold obtained using unsupervised algorithms. Each point in our manifold is a neuron; nearby neurons respond similarly in time to similar parts of a stimulus ensemble. This ensemble includes drifting gratings and flows, i.e., patterns resembling what a mouse would “see” running through fields. Regarding (i), our manifold differs from the standard practice in computational neuroscience: embedding trials in neural coordinates. Topology matters: we infer that, if the circuit consists of separate components, the manifold is discontinuous (illustrated with retinal data). If there is significant overlap between circuits, the manifold is nearly-continuous (cortical data). Regarding (ii), most of the cortical manifold is not activated with conventional gratings, despite their prominence in laboratory settings. Our manifold suggests organizing cortical circuitry by a few specialized circuits for specific members of the stimulus ensemble, together with circuits involving ‘multi-stimuli’-responding neurons. To approach real circuits, local neighborhoods in the manifold are identified with actual circuit components. For retinal data, we show these components correspond to distinct ganglion cell types by their mosaic-like receptive field organization, while for cortical data, neighborhoods organize neurons by type (excitatory/inhibitory) and anatomical layer. In summary: the topology of neural organization reflects well the underlying anatomy and physiology of the retina and the visual cortex

Gli1 enhances migration and invasion via up-regulation of MMP-11 and promotes metastasis in ERα negative breast cancer cell lines

Gli1 is an established oncogene and its expression in Estrogen Receptor (ER) α negative and triple negative breast cancers is predictive of a poor prognosis; however, the biological functions regulated by Gli1 in breast cancer have not been extensively evaluated. Herein, Gli1 was over-expressed or down-regulated (by RNA interference and by expression of the repressor form of Gli3) in the ERα negative, human breast cancer cell lines MDA-MB-231 and SUM1315. Reduced expression of Gli1 in these two cell lines resulted in a decrease in migration and invasion. Gli1 over-expression increased the migration and invasion of MDA-MB-231 cells with a corresponding increase in expression of MMP-11. Silencing MMP-11 in MDA-MB-231 cells that over-expressed Gli1 abrogated the Gli1-induced enhancement of migration and invasion. Sustained suppression of Gli1 expression decreased growth of MDA-MB-231 in vitro by increasing apoptosis and decreasing proliferation. In addition, silencing of Gli1 reduced the numbers and sizes of pulmonary metastases of MDA-MB-231 in an in vivo experimental metastasis assay. In summary, Gli1 promotes the growth, survival, migration, invasion and metastasis of ERα negative breast cancer. Additionally, MMP-11 is up-regulated by Gli1 and mediates the migration and invasion induced by Gli1 in MDA-MB-231