Energy of Isolated Systems at Retarded Times as the Null Limit of Quasilocal Energy

We define the energy of a perfectly isolated system at a given retarded time as the suitable null limit of the quasilocal energy $E$. The result coincides with the Bondi-Sachs mass. Our $E$ is the lapse-unity shift-zero boundary value of the gravitational Hamiltonian appropriate for the partial system $\Sigma$ contained within a finite topologically spherical boundary $B = \partial \Sigma$. Moreover, we show that with an arbitrary lapse and zero shift the same null limit of the Hamiltonian defines a physically meaningful element in the space dual to supertranslations. This result is specialized to yield an expression for the full Bondi-Sachs four-momentum in terms of Hamiltonian values.Comment: REVTEX, 16 pages, 1 figur

World Mineral Production 2011-15

The latest edition of this annual publication from the British Geological Survey (BGS). This volume contains mineral production statistics for the five year period from 2011 to 2015, for more than 70 mineral commodities, by country worldwide. It is the latest publication from the World Mineral Statistics dataset which began in 1913. The information contained in the dataset, and associated publications, is compiled from a wide range of sources: home and overseas government departments, national statistical offices, specialist commodity authorities, company reports, and a network of contacts throughout the world. The database compilers aim for integrity and accuracy in the data and, for quality control purposes, participate in international specialist groups, and maintain close links with other mineral statistics providers in Europe and North America

World Mineral Production 2012-16

The latest edition of this annual publication from the British Geological Survey (BGS) is now available to download. This volume contains mineral production statistics for the five year period from 2012 to 2016, for more than 70 mineral commodities, by country worldwide. Additional tables containing European production of aggregates and cement are included as an Appendix. It is the latest publication from the World Mineral Statistics dataset which began in 1913. The information contained in the dataset, and associated publications, is compiled from a wide range of sources: home and overseas government departments, national statistical offices, specialist commodity authorities, company reports, and a network of contacts throughout the world

World Mineral Production 2009-13

The latest edition of this annual publication from the British Geological Survey (BGS) is now available to download. This volume contains mineral production statistics for the five year period from 2009 to 2013, for more than 70 mineral commodities, by country worldwide. It is the latest publication from the World Mineral Statistics dataset which began in 1913. The information contained in the dataset, and associated publications, is compiled from a wide range of sources: home and overseas government departments, national statistical offices, specialist commodity authorities, company reports, and a network of contacts throughout the world. The database compilers aim for integrity and accuracy in the data and, for quality control purposes, participate in international specialist groups, and maintain close links with other mineral statistics providers in Europe and North America. The data provides essential mineral intelligence for: • security of supply issues • economic analyses • environmental issues • sustainable development planning • regulation and policy issues • commercial strategic planning The data are available in the following formats: • Annual publication of “World Mineral Production” and its predecessors, which can be downloaded in pdf from our World Archive • MS Excel for years from 1992 via our data download tool • The most recent editions are available to purchase in hard copy from the BGS online shop • One off reports such as those shown lower down this page, available for download in pd

World mineral production 2010-14

The latest edition of this annual publication from the British Geological Survey (BGS). This volume contains mineral production statistics for the five year period from 2010 to 2014, for more than 70 mineral commodities, by country worldwide. It is the latest publication from the World Mineral Statistics dataset which began in 1913. The information contained in the dataset, and associated publications, is compiled from a wide range of sources: home and overseas government departments, national statistical offices, specialist commodity authorities, company reports, and a network of contacts throughout the world. The database compilers aim for integrity and accuracy in the data and, for quality control purposes, participate in international specialist groups, and maintain close links with other mineral statistics providers in Europe and North America

The influence of hypoxia and energy depletion on the response of endothelial cells to the vascular disrupting agent combretastatin A-4-phosphate

Combretastatin A-4 phosphate (CA4P) is a microtubule-disrupting tumour-selective vascular disrupting agent (VDA). CA4P activates the actin-regulating RhoA-GTPase/ ROCK pathway, which is required for full vascular disruption. While hypoxia renders tumours resistant to many conventional therapies, little is known about its influence on VDA activity. Here, we found that active RhoA and ROCK effector phospho-myosin light chain (pMLC) were downregulated in endothelial cells by severe hypoxia. CA4P failed to activate RhoA/ROCK/pMLC but its activity was restored upon reoxygenation. Hypoxia also inhibited CA4P-mediated actinomyosin contractility, VE-cadherin junction disruption and permeability rise. Glucose withdrawal downregulated pMLC, and coupled with hypoxia, reduced pMLC faster and more profoundly than hypoxia alone. Concurrent inhibition of glycolysis (2-deoxy-D-glucose, 2DG) and mitochondrial respiration (rotenone) caused profound actin filament loss, blocked RhoA/ROCK signalling and rendered microtubules CA4P-resistant. Withdrawal of the metabolism inhibitors restored the cytoskeleton and CA4P activity. The AMP-activated kinase AMPK was investigated as a potential mediator of pMLC downregulation. Pharmacological AMPK activators that generate AMP, unlike allosteric activators, downregulated pMLC but only when combined with 2DG and/or rotenone. Altogether, our results suggest that Rho/ROCK and actinomyosin contractility are regulated by AMP/ATP levels independently of AMPK, and point to hypoxia/energy depletion as potential modifiers of CA4P response

Playing with the future: social irrealism and the politics of aesthetics

In this paper we wish to explore the political possibilities of video games. Numerous scholars now take seriously the place of popular culture in the remaking of our geographies, but video games still lag behind. For us, this tendency reflects a general response to them as imaginary spaces that are separate from everyday life and 'real' politics. It is this disconnect between abstraction and lived experience that we complicate by defining play as an event of what Brian Massumi calls lived abstraction. We wish to short-circuit the barriers that prevent the aesthetic resonating with the political and argue that through their enactment, video games can animate fantastical futures that require the player to make, and reflect upon, profound ethical decisions that can be antagonistic to prevailing political imaginations. We refer to this as social irrealism to demonstrate that reality can be understood through the impossible and the imagined

Clinically Silent Alzheimer\u27s and Vascular Pathologies Influence Brain Networks Supporting Executive Function in Healthy Older Adults

Aging is associated with declines in executive function. We examined how executive functional brain systems are influenced by clinically silent Alzheimer’s disease (AD) pathology and cerebral white matter hyperintensities (WMHs). Twenty-nine younger adults and thirty-four cognitively normal older adults completed a working memory paradigm while functional magnetic resonance imaging (fMRI) was performed. Older adults further underwent lumbar cerebrospinal fluid (CSF) draw for assessment of AD pathology and FLAIR imaging for assessment of WMHs. Accurate working memory performance in both age groups was associated with high fronto-visual functional connectivity (fC). However, in older adults, higher expression of fronto-visual fC was linked with lower levels of clinically silent AD pathology. In addition, AD pathology and WMHs were each independently related to increased fMRI response in the left dorsolateral prefrontal cortex, a pattern associated with slower task performance. Our results suggest that clinically silent AD pathology is related to lower expression of a fronto-visual fC pattern supporting executive task performance. Further, our findings suggest that AD pathology and WMHs appear to be linked with ineffective increases in frontal response in CN older adults

KLF9 and JNK3 Interact to Suppress Axon Regeneration in the Adult CNS

Neurons in the adult mammalian CNS decrease in intrinsic axon growth capacity during development in concert with changes in Krüppel-like transcription factors (KLFs). KLFs regulate axon growth in CNS neurons including retinal ganglion cells (RGCs). Here, we found that knock-down of KLF9, an axon growth suppressor that is normally upregulated 250-fold in RGC development, promotes long-distance optic nerve regeneration in adult rats of both sexes. We identified a novel binding partner, MAPK10/JNK3 kinase, and found that JNK3 (c-Jun N-terminal kinase 3) is critical for KLF9\u27s axon-growth-suppressive activity. Interfering with a JNK3-binding domain or mutating two newly discovered serine phosphorylation acceptor sites, Ser106 and Ser110, effectively abolished KLF9\u27s neurite growth suppression in vitro and promoted axon regeneration in vivo. These findings demonstrate a novel, physiologic role for the interaction of KLF9 and JNK3 in regenerative failure in the optic nerve and suggest new therapeutic strategies to promote axon regeneration in the adult CNS