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\"Critical questions of purpose, quality, choice, and access in public education have been key in processes of neoliberal globalization spanning the last four decades. The growing privatization of schools around the world has resulted in fundamental changes regarding the ways in which local systems of education are imagined and re-constructed. Schools and schooling are now increasingly (re)fashioned in alignment with global neoliberal imaginaries for the purpose of (re)producing human capital in the service of private interests. As a result, education for social betterment and democratic engagement, two pillars of public school policies throughout the 20th century, are compromised, even undermined. Employing models and research findings from critical international political economy and progressive education, Globalization and the Neoliberal Schoolhouse: Education in a World of Trouble explores the corrosive influences of commodification and privatization on public education worldwide, within the context of crisis-ridden neoliberal globalization and expanding global capitalist governance. The consequences are nation-state de-evolution, social and cultural decay, and the forfeiture of public schools as engines of progress. Understanding how the historical emergence, political economic processes, and governing institutions of neoliberal globalization are adversely impacting local systems of education - and what to do about it - is important to free education advocates, civic-minded educators, student teachers, social activists, and education development specialists everywhere!\"-- Provided by publisher.

Nutritional status provides metabolic substrates to activate AMP-Activated Protein Kinase (AMPK), the energy sensor that regulates metabolism. Recent evidence has demonstrated that AMPK has wider functions with respect to regulating immune cell metabolism and function. One such example is the regulatory role that AMPK has on NLRP3-inlflammasome and IL-1β biology. This in turn can result in subsequent negative downstream effects on glucose, lipid and insulin metabolism. Nutrient stress in the form of obesity can impact AMPK and whole-body metabolism, leading to complications such as type 2 diabetes and cancer risk. There is a lack of data regarding the nature and extent that nutrient status has on AMPK and metabolic-inflammation. However, emerging work elucidates to a direct role of individual nutrients on AMPK and metabolic-inflammation, as a possible means of modulating AMPK activity. The posit being to use such nutritional agents to re-configure metabolic-inflammation towards more oxidative phosphorylation and promote the resolution of inflammation. The complex paradigm will be discussed within the context of if/how dietary components, nutrients including fatty acids and non-nutrient food components, such as resveratrol, berberine, curcumin and the flavonoid genistein, modulate AMPK dependent processes relating to inflammation and metabolism.

\"Altera Roma explores the confrontation of two cultures--European and Amerindian--and two empires--Spanish and Aztec. In an age of exploration and conquest, Spanish soldiers, missionaries, and merchants brought an array of cultural preconceptions. Their encounter with Aztec civilization coincided with Europe's rediscovery of classical antiquity, and Tenochtitlâan came to be regarded a 'second Rome, ' altera Roma. Iberia's past as the Roman province of Hispania served to both guide and critique the Spanish overseas mission. The dialogue that emerged between the Old World and the New World shaped a dual heritage into the unique culture of Nueva Espaنna. In this volume, 10 eminent historians and archaeologists examine the analogies between empires widely separated in time and place, and consider how monumental art and architecture created 'theater states, ' a strategy that links ancient Rome, Hapsburg Spain, preconquest Mexico, and other imperial regimes\"--Provided by publisher.

The lowest-energy exciton state in caesium lead halide perovskite nanocrystals is shown to be a bright triplet state, contrary to expectations that lowest-energy excitons should always be dark. A bright future for semiconductors Lead halide perovskite semiconductor nanocrystals are attracting considerable interest as materials for solar cells and light-emitting diodes because of their excellent photophysical properties. But what makes them so special? Excitons are the electronic excitations that are ultimately responsible for the emissive properties of nanostructured semiconductors, and prevailing wisdom is that the lowest-energy excitonic state will be long-lived and hence poorly emitting (or 'dark'). Michael Becker et al . now show that caesium lead halide perovskites disobey this rule: the lowest-energy excitons are instead unusually 'bright', emitting much faster than any other semiconductor nanocrystal. Furthermore, they identify the structural and electronic factors responsible for this anomalous behaviour, providing vital clues for the identification of other semiconducting materials that might behave similarly. Nanostructured semiconductors emit light from electronic states known as excitons 1 . For organic materials, Hund’s rules 2 state that the lowest-energy exciton is a poorly emitting triplet state. For inorganic semiconductors, similar rules 3 predict an analogue of this triplet state known as the ‘dark exciton’ 4 . Because dark excitons release photons slowly, hindering emission from inorganic nanostructures, materials that disobey these rules have been sought. However, despite considerable experimental and theoretical efforts, no inorganic semiconductors have been identified in which the lowest exciton is bright. Here we show that the lowest exciton in caesium lead halide perovskites (CsPbX 3 , with X = Cl, Br or I) involves a highly emissive triplet state. We first use an effective-mass model and group theory to demonstrate the possibility of such a state existing, which can occur when the strong spin–orbit coupling in the conduction band of a perovskite is combined with the Rashba effect 5 , 6 , 7 , 8 , 9 , 10 . We then apply our model to CsPbX 3 nanocrystals 11 , and measure size- and composition-dependent fluorescence at the single-nanocrystal level. The bright triplet character of the lowest exciton explains the anomalous photon-emission rates of these materials, which emit about 20 and 1,000 times faster 12 than any other semiconductor nanocrystal at room 13 , 14 , 15 , 16 and cryogenic 4 temperatures, respectively. The existence of this bright triplet exciton is further confirmed by analysis of the fine structure in low-temperature fluorescence spectra. For semiconductor nanocrystals, which are already used in lighting 17 , lasers 18 and displays 19 , these excitons could lead to materials with brighter emission. More generally, our results provide criteria for identifying other semiconductors that exhibit bright excitons, with potential implications for optoelectronic devices.

Recent developments in theoretical techniques have significantly improved the predictive power of density-functional-based calculations. In this review, we discuss how such advancements have enabled improved understanding of native point defects in GaN. We review the methodologies for the calculation of point defects, and discuss how techniques for overcoming the band-gap problem of density functional theory affect native defect calculations. In particular, we examine to what extent calculations performed with semilocal functionals (such as the generalized gradient approximation), combined with correction schemes, can produce accurate results. The properties of vacancy, interstitial, and antisite defects in GaN are described, as well as their interaction with common impurities. We also connect the first-principles results to experimental observations, and discuss how native defects and their complexes impact the performance of nitride devices. Overall, we find that lower-cost functionals, such as the generalized gradient approximation, combined with band-edge correction schemes can produce results that are qualitatively correct. However, important physics may be missed in some important cases, particularly for optical transitions and when carrier localization occurs.

Apolipoprotein A-I (ApoA-I), the primary component of high-density lipoprotein (HDL) cholesterol primes β-cells to increase insulin secretion, however, the mechanisms involved are not fully defined. Here, we aimed to confirm ApoA-I receptors in β-cells and delineate ApoA-I-receptor pathways in β-cell insulin output. An LRC-TriCEPS experiment was performed using the INS-1E rat β-cell model and ApoA-I for unbiased identification of ApoA-I receptors. Identified targets, alongside ATP binding cassette transporter A1 (ABCA1) (included control) were silenced in the same cells, and insulin secretion (ELISA) and mitochondrial metabolism (seahorse) were assessed with/without ApoA-I priming. Human β-cell expression data was used to investigate ApoA-I receptor pathways in type 2 diabetes (T2D). Scavenger receptor B1 (SR-BI) and regulator of microtubule dynamics 1 were identified as ApoA-I targets. SR-BI or ABCA1 silencing abolished ApoA-I induced increases in insulin secretion. ApoA-I priming increased mitochondrial OXPHOS, however this was greatly attenuated with SR-BI or ABCA1 silencing. Supporting this, human β-cell expression data investigations found SR-BI and ABCA1 to be correlated with genes associated with mitochondrial pathways. In all, SR-BI and ABCA1 correlated with 73 and 3 genes differentially expressed in T2D, respectively. We confirm that SR-BI and ABCA1 are the primary β-cell ApoA-I receptors and demonstrate that ApoA-I priming enhances β-cell insulin secretion via the upregulation of mitochondrial metabolism through ApoA-I-SR-BI and ApoA-I-ABCA1 pathways. We propose that SR-BI relies on mitochondrial and exocytotic pathways, while ABCA1 depends solely on mitochondrial pathways. Our findings uncover new targets in ApoA-I β-cell mechanism for T2D therapies.

The difficulty in obtaining as well as maintaining weight loss, together with the impairment of metabolic control in conditions like diabetes and cardiovascular disease, may represent pathological situations of inadequate neural communication between the brain and peripheral organs and tissues. Innervation of adipose tissues by peripheral nerves provides a means of communication between the master metabolic regulator in the brain (chiefly the hypothalamus), and energy-expending and energy-storing cells in the body (primarily adipocytes). Although chemical and surgical denervation studies have clearly demonstrated how crucial adipose tissue neural innervation is for maintaining proper metabolic health, we have uncovered that adipose tissue becomes neuropathic (ie: reduction in neurites) in various conditions of metabolic dysregulation. Here, utilizing both human and mouse adipose tissues, we present evidence of adipose tissue neuropathy, or loss of proper innervation, under pathophysiological conditions such as obesity, diabetes, and aging, all of which are concomitant with insult to the adipose organ as well as metabolic dysfunction. Neuropathy is indicated by loss of nerve fiber protein expression, reduction in synaptic markers, and lower neurotrophic factor expression in adipose tissue. Aging-related adipose neuropathy particularly results in loss of innervation around the tissue vasculature, which cannot be reversed by exercise. Together with indications of neuropathy in muscle and bone, these findings underscore that peripheral neuropathy is not restricted to classic tissues like the skin of distal extremities, and that loss of innervation to adipose may trigger or exacerbate metabolic diseases. In addition, we have demonstrated stimulation of adipose tissue neural plasticity with cold exposure, which may ameliorate adipose neuropathy and be a potential therapeutic option to re-innervate adipose and restore metabolic health.

A critical, long‐standing problem in substorm research is identification of the sequence of events leading to substorm auroral onset. Based on event and statistical analysis of THEMIS all‐sky imager data, we show that there is a distinct and repeatable sequence of events leading to onset, the sequence having similarities to and important differences from previous ideas. The sequence is initiated by a poleward boundary intensification (PBI) and followed by a north‐south (N‐S) arc moving equatorward toward the onset latitude. Because of the linkage of fast magnetotail flows to PBIs and to N‐S auroras, the results indicate that onset is preceded by enhanced earthward plasma flows associated with enhanced reconnection near the pre‐existing open‐closed field line boundary. The flows carry new plasma from the open field line region to the plasma sheet. The auroral observations indicate that Earthward‐transport of the new plasma leads to a near‐Earth instability and auroral breakup ∼5.5 min after PBI formation. Our observations also indicate the importance of region 2 magnetosphere‐ionosphere electrodynamic coupling, which may play an important role in the motion of pre‐onset auroral forms and determining the local times of onsets. Furthermore, we find motion of the pre‐onset auroral forms around the Harang reversal and along the growth phase arc, reflecting a well‐developed region 2 current system within the duskside convection cell, and also a high probability of diffuse‐appearing aurora occurrence near the onset latitude, indicating high plasma pressure along these inner plasma sheet field lines, which would drive large region 2 currents.