Making it real: exploring the potential of Augmented Reality for teaching primary school science

The use of Augmented Reality (AR) in formal education could prove a key component in future learning environments that are richly populated with a blend of hardware and software applications. However, relatively little is known about the potential of this technology to support teaching and learning with groups of young children in the classroom. Analysis of teacher-child dialogue in a comparative study between use of an AR virtual mirror interface and more traditional science teaching methods for 10-year-old children, revealed that the children using AR were less engaged than those using traditional resources. We suggest four design requirements that need to be considered if AR is to be successfully adopted into classroom practice. These requirements are: flexible content that teachers can adapt to the needs of their children, guided exploration so learning opportunities can be maximised, in a limited time, and attention to the needs of institutional and curricular requirements

PI3Ks Maintain the Structural Integrity of T-Tubules in Cardiac Myocytes

Phosphoinositide 3-kinases (PI3Ks) regulate numerous physiological processes including some aspects of cardiac function. Although regulation of cardiac contraction by individual PI3K isoforms has been studied, little is known about the cardiac consequences of downregulating multiple PI3Ks concurrently.Genetic ablation of both p110α and p110β in cardiac myocytes throughout development or in adult mice caused heart failure and death. Ventricular myocytes from double knockout animals showed transverse tubule (T-tubule) loss and disorganization, misalignment of L-type Ca(2+) channels in the T-tubules with ryanodine receptors in the sarcoplasmic reticulum, and reduced Ca(2+) transients and contractility. Junctophilin-2, which is thought to tether T-tubules to the sarcoplasmic reticulum, was mislocalized in the double PI3K-null myocytes without a change in expression level.PI3K p110α and p110β are required to maintain the organized network of T-tubules that is vital for efficient Ca(2+)-induced Ca(2+) release and ventricular contraction. PI3Ks maintain T-tubule organization by regulating junctophilin-2 localization. These results could have important medical implications because several PI3K inhibitors that target both isoforms are being used to treat cancer patients in clinical trials

The political economy of the divine

Susan Feiner\u27s paper demonstrates the connection between the inner logic and the concerns of the Hebrew bible, and the central market metaphor of contemporary mainstream economics. They have overlapping concerns, they both establish taboos that are essential to \u27right living\u27, and both the bible and public policy seek to sustain the existing social/sexual order. As a result, the market of mainstream economics resembles the biblical figure \u27Yahweh\u27. This explains the staying power of mainstream economics: consumers of mainstream economics are seduced by the hidden likeness to sacred text

AKIP1 Expression Modulates Mitochondrial Function in Rat Neonatal Cardiomyocytes

<p>A kinase interacting protein 1 (AKIP1) is a molecular regulator of protein kinase A and nuclear factor kappa B signalling. Recent evidence suggests AKIP1 is increased in response to cardiac stress, modulates acute ischemic stress response, and is localized to mitochondria in cardiomyocytes. The mitochondrial function of AKIP1 is, however, still elusive. Here, we investigated the mitochondrial function of AKIP1 in a neonatal cardiomyocyte model of phenylephrine (PE)-induced hypertrophy. Using a seahorse flux analyzer we show that PE stimulated the mitochondrial oxygen consumption rate (OCR) in cardiomyocytes. This was partially dependent on PE mediated AKIP1 induction, since silencing of AKIP1 attenuated the increase in OCR. Interestingly, AKIP1 overexpression alone was sufficient to stimulate mitochondrial OCR and in particular ATP-linked OCR. This was also true when pyruvate was used as a substrate, indicating that it was independent of glycolytic flux. The increase in OCR was independent of mitochondrial biogenesis, changes in ETC density or altered mitochondrial membrane potential. In fact, the respiratory flux was elevated per amount of ETC, possibly through enhanced ETC coupling. Furthermore, overexpression of AKIP1 reduced and silencing of AKIP1 increased mitochondrial superoxide production, suggesting that AKIP1 modulates the efficiency of electron flux through the ETC. Together, this suggests that AKIP1 overexpression improves mitochondrial function to enhance respiration without excess superoxide generation, thereby implicating a role for AKIP1 in mitochondrial stress adaptation. Upregulation of AKIP1 during different forms of cardiac stress may therefore be an adaptive mechanism to protect the heart.</p>