University of Arizona

About: University of Arizona is a education organization based out in Tucson, Arizona, United States. It is known for research contribution in the topics: Population & Galaxy. The organization has 63805 authors who have published 155998 publications receiving 6854915 citations. The organization is also known as: UA & U of A.

Use and Abuse of Reusable Learning Objects

Abstract: The term Learning Object, first popularized by Wayne Hodgins in 1994 when he named the CedMA working group "Learning Architectures, APIs and Learning Objects", has become the Holy Grail of content creation and aggregation in the computer-mediated learning field. The terms Learning Objects (LOs) and Reusable Learning Objects are frequently employed in uncritical ways, thereby reducing them to mere slogans. The serious lack of conceptual clarity and reflection is evident in the multitude of definitions and uses of LOs. The objectives of this paper are to assess current definitions of the term Learning Object, to articulate the foundational principles for developing a concept of LOs, and to provide a methodology and broad set of guidelines for creating LOs.

Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children

Abstract: Among 419 participants who underwent randomization (at which point 73% had moderate or severe disease), omalizumab as compared with placebo significantly reduced the number of days with asthma symptoms, from 1.96 to 1.48 days per 2-week interval, a 24.5% decrease (P<0.001). Similarly, omalizumab significantly reduced the proportion of participants who had one or more exacerbations from 48.8 to 30.3% (P<0.001). Improvements occurred with omalizumab despite reductions in the use of inhaled glucocorticoids and long-acting beta-agonists. Conclusions When added to a regimen of guidelines-based therapy for inner-city children, adolescents, and young adults, omalizumab further improved asthma control, nearly eliminated seasonal peaks in exacerbations, and reduced the need for other medications to control asthma. (Funded by the National Institute of Allergy and Infectious Diseases and Novartis; ClinicalTrials.gov number, NCT00377572.)

Whatever Happened to the Jock, the Brain, and the Princess? Young Adult Pathways Linked to Adolescent Activity Involvement and Social Identity.

Abstract: This study examined young adult sequelae of participation in high school activities and identity group for 900 participants from the Michigan Study of Life Transitions.Participation at Grade 10 in high school activities predicted later substance use, psychological adjustment, and educational and occupational outcomes.Prosocial activity participation predicted lower substance use and higher self-esteem and an increased likelihood of college graduation.Performing arts participation predicted more years of education as well as increases in drinking between ages 18 and 21 and higher rates of suicide attempts and psychologist visits by the age of 24.Sports participation predicted positive educational and occupational outcomes and lower levels of social isolation but also higher rates of drinking. Breakfast Club identity categories were predictive of both levels and longitudinal patterns in substance use, education and work outcomes, and psychological adjustment.In general, Jocks and Brains showed the most posi...

The Arabidopsis SOS2 protein kinase physically interacts with and is activated by the calcium-binding protein SOS3

Abstract: The Arabidopsis thaliana SOS2 and SOS3 genes are required for intracellular Na+ and K+ homeostasis and plant tolerance to high Na+ and low K+ environments. SOS3 is an EF hand type calcium-binding protein having sequence similarities with animal neuronal calcium sensors and the yeast calcineurin B. SOS2 is a serine/threonine protein kinase in the SNF1/AMPK family. We report here that SOS3 physically interacts with and activates SOS2 protein kinase. Genetically, sos2sos3 double mutant analysis indicates that SOS2 and SOS3 function in the same pathway. Biochemically, SOS2 interacts with SOS3 in the yeast two-hybrid system and in vitro binding assays. The interaction is mediated by the C-terminal regulatory domain of SOS2. SOS3 activates SOS2 protein kinase activity in a Ca2+-dependent manner. Therefore, SOS3 and SOS2 define a novel regulatory pathway important for the control of intracellular ion homeostasis and salt tolerance in plants.

Acid-Mediated Tumor Invasion: a Multidisciplinary Study

Abstract: The acid-mediated tumor invasion hypothesis proposes altered glucose metabolism and increased glucose uptake, observed in the vast majority of clinical cancers by fluorodeoxyglucose-positron emission tomography, are critical for development of the invasive phenotype. In this model, increased acid production due to altered glucose metabolism serves as a key intermediate by producing H(+) flow along concentration gradients into adjacent normal tissue. This chronic exposure of peritumoral normal tissue to an acidic microenvironment produces toxicity by: (a) normal cell death caused by the collapse of the transmembrane H(+) gradient inducing necrosis or apoptosis and (b) extracellular matrix degradation through the release of cathepsin B and other proteolytic enzymes. Tumor cells evolve resistance to acid-induced toxicity during carcinogenesis, allowing them to survive and proliferate in low pH microenvironments. This permits them to invade the damaged adjacent normal tissue despite the acid gradients. Here, we describe theoretical and empirical evidence for acid-mediated invasion. In silico simulations using mathematical models provide testable predictions concerning the morphology and cellular and extracellular dynamics at the tumor-host interface. In vivo experiments confirm the presence of peritumoral acid gradients as well as cellular toxicity and extracellular matrix degradation in the normal tissue exposed to the acidic microenvironment. The acid-mediated tumor invasion model provides a simple mechanism linking altered glucose metabolism with the ability of tumor cells to form invasive cancers.