How to Conduct Cloud-Based Student Labs in Your Classroom

This workshop uses hands-on exercises to show participants how the cloud can be an effective and cost-saving platform for student laboratory exercises. Participants will learn how to create their own virtual computer on Amazon\u27s cloud platform, then use the server to 1) publish their own web site and 2) run a short molecular modeling simulation using the PSI4 software, all in just a few minutes. We will also show participants how to find and decipher cloud platform pricing models, for a better idea of how much cloud computing will cost instructors and/or their students. Note: An Amazon\u27s AWS free tier account (http://aws.amazon.com/free/) will be required to participate in the workshop. The workshop will only use free tier services, so attendees will not incur any costs for participating. We strongly recommend you sign up a few days prior to the workshop. Amazon AWS does not typically have instant approval for new customers

Freire re-viewed

The work of Paulo Freire is associated with themes of oppression and liberation, and his critical pedagogy is visionary in its attempts to bring about social transformation. Freire has created a theory of education that embeds these issues within social relations that center around both ideological and material domination. In this review essay, Sue Jackson explores three books: Freire’s final work Pedagogy of Indignation; Cesar Augusto Rossatto’s Engaging Paulo Freire’s Pedagogy of Possibility, which attempts to engage Freire’s pedagogy of possibility; and C.A. Bowers and Frederique Apffel-Marglin’s edited collection Re-thinking Freire, which asks readers to reconsider Freire’s work in light of globalization and environmental crises. Jackson questions the extent to which Freire’s pedagogical approaches are useful to educators as well as to “the oppressed,” and whether challenges to re-think Freire can lead to new kinds of critical pedagogies

Organ Size Control by Hippo and TOR Pathways

The determination of final organ size is a highly coordinated and complex process that relies on the precise regulation of cell number and/or cell size. Perturbation of organ size control contributes to many human diseases, including hypertrophy, degenerative diseases, and cancer. Hippo and TOR are among the key signaling pathways involved in the regulation of organ size through their respective functions in the regulation of cell number and cell size. Here, we review the general mechanisms that regulate organ growth, describe how Hippo and TOR control key aspects of growth, and discuss recent findings that highlight a possible coordination between Hippo and TOR in organ size regulation

Class III PI3K regulates organismal glucose homeostasis by providing negative feedback on hepatic insulin signalling.

Defective hepatic insulin receptor (IR) signalling is a pathogenic manifestation of metabolic disorders including obesity and diabetes. The endo/lysosomal trafficking system may coordinate insulin action and nutrient homeostasis by endocytosis of IR and the autophagic control of intracellular nutrient levels. Here we show that class III PI3K--a master regulator of endocytosis, endosomal sorting and autophagy--provides negative feedback on hepatic insulin signalling. The ultraviolet radiation resistance-associated gene protein (UVRAG)-associated class III PI3K complex interacts with IR and is stimulated by insulin treatment. Acute and chronic depletion of hepatic Vps15, the regulatory subunit of class III PI3K, increases insulin sensitivity and Akt signalling, an effect that requires functional IR. This is reflected by FoxO1-dependent transcriptional defects and blunted gluconeogenesis in Vps15 mutant cells. On depletion of Vps15, the metabolic syndrome in genetic and diet-induced models of insulin resistance and diabetes is alleviated. Thus, feedback regulation of IR trafficking and function by class III PI3K may be a therapeutic target in metabolic conditions of insulin resistance

Extremely Metal-Poor Stars. VII. The Most Metal-Poor Dwarf, CS 22876-032

We report high-resolution, high-signal-to-noise, observations of the extremely metal-poor double-lined spectroscopic binary CS 22876-032. The system has a long period : P = 424.7 $\pm$ 0.6 days. It comprises two main sequence stars having effective temperatures 6300 K and 5600 K, with a ratio of secondary to primary mass of 0.89 $\pm$ 0.04. The metallicity of the system is [Fe/H] = -3.71 $\pm$ 0.11 $\pm$ 0.12 (random and systematic errors) -- somewhat higher than previous estimates. We find [Mg/Fe] = 0.50, typical of values of less extreme halo material. [Si/Fe], [Ca/Fe], and [Ti/Fe], however, all have significantly lower values, ~ 0.0-0.1, suggesting that the heavier elements might have been underproduced relative to Mg in the material from which this object formed. In the context of the hypothesis that the abundance patterns of extremely metal-poor stars are driven by individual enrichment events and the models of Woosley and Weaver (1995), the data for CS 22876-032 are consistent with its having been enriched by a zero-metallicity supernova of mass 30 M$_{\odot}$. As the most metal-poor near-main-sequence-turnoff star currently known, the primary of the system has the potential to strongly constrain the primordial lithium abundance. We find A(Li) (= log(N(Li)/N(H)) + 12.00) = 2.03 $\pm$ 0.07, which is consistent with the finding of Ryan et al. (1999) that for stars of extremely low metallicity A(Li) is a function of [Fe/H].Comment: 27 pages, 9 figures, accepted for publication in The Astrophysical Journal, Sept. 1, 2000 issu

Rag GTPases are cardioprotective by regulating lysosomal function.

The Rag family proteins are Ras-like small GTPases that have a critical role in amino-acid-stimulated mTORC1 activation by recruiting mTORC1 to lysosome. Despite progress in the mechanistic understanding of Rag GTPases in mTORC1 activation, little is known about the physiological function of Rag GTPases in vivo. Here we show that loss of RagA and RagB (RagA/B) in cardiomyocytes results in hypertrophic cardiomyopathy and phenocopies lysosomal storage diseases, although mTORC1 activity is not substantially impaired in vivo. We demonstrate that despite upregulation of lysosomal protein expression by constitutive activation of the transcription factor EB (TFEB) in RagA/B knockout mouse embryonic fibroblasts, lysosomal acidification is compromised owing to decreased v-ATPase level in the lysosome fraction. Our study uncovers RagA/B GTPases as key regulators of lysosomal function and cardiac protection

Sensitive and specific discrimination of pathogenic and nonpathogenic Escherichia coli using Raman spectroscopy - a comparison of two multivariate analysis techniques

The determination of bacterial identity at the strain level is still a complex and time-consuming endeavor. In this study, visible wavelength spontaneous Raman spectroscopy has been used for the discrimination of four closely related Escherichia coli strains: pathogenic enterohemorrhagic E. coli O157:H7 and non-pathogenic E. coli C, E. coli Hfr K-12, and E. coli HF4714. Raman spectra from 600 to 2000 cm-1 were analyzed with two multivariate chemometric techniques, principal component-discriminant function analysis and partial least squares-discriminant analysis, to determine optimal parameters for the discrimination of pathogenic E. coli from the non-pathogenic strains. Spectral preprocessing techniques such as smoothing with windows of various sizes and differentiation were investigated. The sensitivity and specificity of both techniques was in excess of 95%, determined by external testing of the chemometric models. This study suggests that spontaneous Raman spectroscopy with visible wavelength excitation is potentially useful for the rapid identification and classification of clinically-relevant bacteria at the strain level

ULK1-mediated phosphorylation of ATG16L1 promotes xenophagy, but destabilizes the ATG16L1 Crohn's mutant.

Autophagy is a highly regulated catabolic pathway that is potently induced by stressors including starvation and infection. An essential component of the autophagy pathway is an ATG16L1-containing E3-like enzyme, which is responsible for lipidating LC3B and driving autophagosome formation. ATG16L1 polymorphisms have been linked to the development of Crohn's disease (CD), and phosphorylation of CD-associated ATG16L1 T300A (caATG16L1) has been hypothesized to contribute to cleavage and autophagy dysfunction. Here we show that ULK1 kinase directly phosphorylates ATG16L1 in response to infection and starvation. Phosphorylated ATG16L1 localizes to the site of internalized bacteria and stable cell lines harbouring a phospho-dead mutant of ATG16L1 have impaired xenophagy, indicating a role for ATG16L1 phosphorylation in the promotion of anti-bacterial autophagy. In contrast to wild-type ATG16L1, ULK1-mediated phosphorylation of caATG16L1 drives its destabilization in response to stress. In summary, our results show that ATG16L1 is a novel target of ULK1 kinase and that ULK1 signalling to ATG16L1 is a double-edged sword, enhancing the function of the wild-type ATG16L1, but promoting degradation of caATG16L1.This work was supported by Canadian Institutes of Health Research (CIHR) Project Grants awarded to RCR (#PJT153034), the UK Dementia Research Institute (funded by MRC, Alzheimer’s Research UK and the Alzheimer’s Society), Wellcome Trust (Principal Research Fellowship to DCR (095317/Z/11/Z), Strategic Grant to Cambridge Institute for Medical Research (100140/Z/12/Z) and studentship to AJ, and the Roger de Spoelberch Foundation. Accademic scholarship from the government of Saudi Arabia (#5976670433) and studentship supported RA. TTL was supported by an Ontario Graduate Scholarship